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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
Biggerstaff, M. et al. (2014) “Estimates of the reproduction number for seasonal, pandemic, and zoonotic influenza: a systematic review of the literature”, BMC Infect Dis 14, 480 (2014).
Brooke, C. B. et al. (2013) “Most Influenza A Virions Fail To Express at Least One Essential Viral Protein”, Journal of Virology Feb 2013, 87 (6) 3155-3162; DOI: 10.1128/JVI.02284-12
Coburn, B. J. et al. (2009) “Modeling influenza epidemics and pandemics: insights into the future of swine flu (H1N1)”, BMC Med 7, 30.
Davies, A. et al. (2013) “Testing the Efficacy of Homemade Masks: Would They Protect in an Influenza Pandemic?”, Disaster Medicine and Public Health Preparedness, Available on CJO 2013 doi:10.1017/dmp.2013.43
Despres, V. R. et al. (2012) “Primary biological aerosol particles in the atmosphere: a review”, Tellus B: Chemical and Physical Meteorology, 64:1, 15598, DOI: 10.3402/tellusb.v64i0.15598
Dowell, S. F. (2001) “Seasonal variation in host susceptibility and cycles of certain infectious diseases”, Emerg Infect Dis. 2001;7(3):369-374. doi:10.3201/eid0703.010301
Hammond, G. W. et al. (1989) “Impact of Atmospheric Dispersion and Transport of Viral Aerosols on the Epidemiology of Influenza”, Reviews of Infectious Diseases, Volume 11, Issue 3, May 1989, Pages 494-497,
Haas, C.N. et al. (1993) “Risk Assessment of Virus in Drinking Water”, Risk Analysis, 13: 545-552. doi:10.1111/j.1539-6924.1993.tb00013.x
HealthKnowlege-UK (2020) “Charter 1a – Epidemiology: Epidemic theory (effective & basic reproduction numbers, epidemic thresholds) & techniques for analysis of infectious disease data (construction & use of epidemic curves, generation numbers, exceptional reporting & identification of significant clusters)”, HealthKnowledge.org.uk, accessed on 2020-04-10.
Lai, A. C. K. et al. (2012) “Effectiveness of facemasks to reduce exposure hazards for airborne infections among general populations”, J. R. Soc. Interface. 9938-948
Leung, N.H.L. et al. (2020) “Respiratory virus shedding in exhaled breath and efficacy of face masks”, Nature Medicine (2020).
Lowen, A. C. et al. (2007) “Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature”, PLoS Pathog 3(10): e151.
Paules, C. and Subbarao, S. (2017) “Influenza”, Lancet, Seminar| Volume 390, ISSUE 10095, P697-708, August 12, 2017.
Sande, van der, M. et al. (2008) “Professional and Home-Made Face Masks Reduce Exposure to Respiratory Infections among the General Population”, PLoS ONE 3(7): e2618. doi:10.1371/journal.pone.0002618 Shaman, J. et al. (2010) “Absolute Humidity and the Seasonal Onset of Influenza in the Continental United States”, PLoS Biol 8(2): e1000316. https://doi.org/10.1371/journal.pbio.1000316
Tracht, S. M. et al. (2010) “Mathematical Modeling of the Effectiveness of Facemasks in Reducing the Spread of Novel Influenza A (H1N1)”, PLoS ONE 5(2): e9018. doi:10.1371/journal.pone.0009018
Viboud C. et al. (2010) “Preliminary Estimates of Mortality and Years of Life Lost Associated with the 2009 A/H1N1 Pandemic in the US and Comparison with Past Influenza Seasons”, PLoS Curr. 2010; 2:RRN1153. Published 2010 Mar 20. doi:10.1371/currents.rrn1153
Wada, K. et al. (2012) “Wearing face masks in public during the influenza season may reflect other positive hygiene practices in Japan”, BMC Public Health 12, 1065 (2012).
Yang, W. et al. (2011) “Concentrations and size distributions of airborne influenza A viruses measured indoors at a health centre, a day-care centre and on aeroplanes”, Journal of the Royal Society, Interface. 2011 Aug;8(61):1176-1184. DOI: 10.1098/rsif.2010.0686.
Yezli, S., Otter, J.A. (2011) “Minimum Infective Dose of the Major Human Respiratory and Enteric Viruses Transmitted Through Food and the Environment”, Food Environ Virol 3, 1-30.
Zwart, M. P. et al. (2009) “An experimental test of the independent action hypothesis in virus-insect pathosystems”, Proc. R. Soc. B. 2762233-2242

https://academic.oup.com/cid/article/65/11/1934/4068747

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.

CITES:

• Association of serum uric acid levels with the progression of Parkinson’s disease in Chinese patients.Sun CC, Luo FF, Wei L, Lei M, Li GF, Liu ZL, LE WD, Xu PY.Chin Med J (Engl). 2012 Feb;125(4):583-7.PMID: 22490478

     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

• Pharmacokinetic-pharmacodynamic modeling of levodopa in patients with advanced Parkinson disease.Adamiak U, Kaldonska M, Klodowska-Duda G, Wyska E, Safranow K, Bialecka M, Gawronska-Szklarz B.Clin Neuropharmacol. 2010 May;33(3):135-41. doi: 10.1097/WNF.0b013e3181d47849.PMID: 20216409 Clinical Trial.
• Four pioneers of L-dopa treatment: Arvid Carlsson, Oleh Hornykiewicz, George Cotzias, and Melvin Yahr.Lees AJ, Tolosa E, Olanow CW.Mov Disord. 2015 Jan;30(1):19-36. doi: 10.1002/mds.26120. Epub 2014 Dec 8.PMID: 25488030 Review.
• Elevated homocysteine levels in levodopa-treated idiopathic Parkinson’s disease: a meta-analysis.Hu XW, Qin SM, Li D, Hu LF, Liu CF.Acta Neurol Scand. 2013 Aug;128(2):73-82. doi: 10.1111/ane.12106. Epub 2013 Feb 21.PMID: 23432663 Review.
• Kornberg H.L. Krebs and his trinity of cycles. Nat. Rev. Mol. Cell Biol. 2000; 1: 225-228

I want you to watch the video above in its entirety before you go on to ask yourself this key question.

Do predatory publishing and social media have something in common that breeds the facade that bad ideas and science can, on the surface contain the aura of truth?

I follow a lot of people on social media who I disagree with because it allows me to see aspects of life I am blinded to by my own biases.  Social media allows me to see things I am blind too because the medium is the message.

When “People” become weak, societies crumble because liberties shrink. Only courageous hearts can endure the bitterness of truth…….

All too often we fail to see the good in a difficult situation. Our minds are wired in such a funny way that we tend to believe just because a door closed it must be a bad thing. I say this because I saw a comment from “progressive author journalist” that said, “Ruth Bader Ginsburg is going to be replaced by a woman who walked through every door that Ginsburg opened for her so she can promptly use her position to shut them all for others behind her.”

When I read the comment above on Twitter and saw how many people liked the comment, I thought to myself, there must be a lot of people on Twitter who think chronically with a closed mind.  These are people who revered RBG in life, but never really understood her message.  Every door was closed to RBG and what did RBG do?  Did she fold like a cheap beach chair or did she do something about it by thinking fiercely about her plight? 

When RBG started law school in 1956, women accounted for less than 3% of the legal profession = CLOSED DOOR

Until the early 1950s, the majority of local school boards and clerical firms had “marriage bar” policies in place against the hiring and retention of married women, so heading off to law school with a family in tow was truly a venture into uncharted waters. This is around the same time when Elinor Ostrom—future Nobel Prize winner in economics—would have been splitting up with her first husband because he saw graduate coursework as incompatible with their life together. This is another example of a CLOSED DOOR.    Did this stop Elinor from creating a new room in the future for women like Ms. Ahern?  What is the common tie here?  In the 1950’s these powerful women did not have social media and that medium was not filtering the way they think into something that create a prison for them so they could not destroy the glass ceilings they faced.

Social media, and specificaly, Ms. Ahern’s tweet, allowed me to realize the basis of our political divide is tied to how people think about ideas when they are unable to process information well. 

History didn’t have to move the direction that it did without some help from thinkers like RBG. Waypavers are willing to be first in line to take chances that others around them are either not willing or not able to. In so doing, they forever alter the expectations of those who come after them. By deciding the path of professional constitutional law was possible for her, Ginsburg made it easier for others to decide they were capable as well.

Ginsburg credited her mother and her undergraduate teachers with enabling her “to take part in the effort to free our daughters and sons to achieve whatever their talents equipped them to accomplish, with no artificial barriers blocking their way” RBG discussed this in her preface of her “In My Own Words”.  She credited her mother with encouraging her to be a lady, meaning, to always be civil; to be independent; and to love libraries and books. It appears this was RBG medium.  That medium bred a different kind of thinking in Justice Ginsburg.  Ginsburg mentioned the ambitious, literary “Jo” from Louisa May Alcott’s Little Women as a favorite find from those early days she spent in the library on page 4 of the book. I suspect if you took a poll of women in business today, you’d find an awful lot of “Jo”s who were also lit on fire by Ms. Alcott.

RBG also credited two of her undergraduate professors, novelist Vladimir Nabokov, and constitutional scholar Robert Cushman, with teaching her the value of choosing words carefully and taking a principled stance.

Justice Ginsburg lived her principles do you think Ms. Ahern does?   Does she value words as an author?  Might that be tied to the medium she trained on?  Do you think that might have some lasting effect on her work because now she is an author and journalist?  Given what RBG said above about words, the door RBG opened, might be fraught with some problems, no?

Don’t judge Ms. Ahern by a tweet, but I want you to ask yourself a question……..might how she saw and learned about RBG on social media define the message she has received and this is now seared into how she acts, speaks, and talks, and will live the rest of her life?  It is quite clear RBG medium was not equivalent to Ms. Ahern’s.  

Why did her tweet about a closed door and RBG go viral on social media?  Might this virus of poor thinking be more dangerous than anything COVID-19 can throw at humanity?

Has social media let a genie out of the bottle that has fostered an anti-wisdom movement that has led to a door that should be bolted shut? 

Why do people believe that this tweet from Ms. Ahern has an aura of truth to it when the life of RBG was all about having a door slammed in her face at every step of her early life?  Wasn’t the action of a slammed door what created a new life for women?    Moreover, those who do believe that Ms. Ahern tweet has some logic to it, how do you think it will affect how they trust Amy Coney Barrett?  How will it affect anyone else in your life who you perceive that closed a door in your face?

It was at that time, I decided I needed to write about this topic in this blog for my patrons to become “agent provocateur” to get you to think about how bad science and poor ideas go viral today and gain traction THEY SHOULD NOT HAVE.  Many of the papers supported by the paradigm on C19 right now have these same traits.  

You don’t believe me? 

Here Fauci explains how and why he will limit who can have in your home, what pets you can have, the end of large events, and the effective dismantlement of cities. This should chill you.

HYPERLINK

This paper shows us how poor science may lead to a tear down of civil liberites.  RBG was a champion of showing this inequity in her legal career.

RBG was deeply concerned about the impact McCarthyism was having on civil liberties in the 1950s. RBG’s engagement with this cause was her first experience with the idea of the lawyer as a defender of constitutional rights, an influence which would carry through into her work with the ACLU’s Women’s Rights Project. The first brief RBG filed with the U.S. Supreme Court as a lawyer was in the 1971 case of Reed v. Reed, in which a mother had sued to be able to administer the estate of her deceased son. Idaho law had given explicit preference to the father since he was male, but the Supreme Court decided in favor of RBG’s argument that the Fourteenth Amendment did protect against gender discrimination in law.

RBG saw this work to advance equality as the “constitutional legacy” of our founding ideals: The founding fathers rebelled against the patriarchal power of kings and the idea that political authority may legitimately rest on birth status. Their culture at their time, she believed, might have held them back from fully perceiving or acting upon ideals of human equality and dignity.  From my reading of RBG life and her legal career this is why she became a leftist.  She was not a progressive or communist in any way.  Today’s leftist have tried to paint her that way to gain a door or access point to put a progressive communist jurist on the SCOTUS.

What really does leftist mean in the world that formed the great mind of RBG?  RBG education ideas were destroyed by her life experiences she faced.  She used those life experiences and chaos to change her world and the world around her.  She realized in law school and in her cases she argued before the SCOTUS that it was the incompleteness of the founding father’s vision of a non-hierarchical liberal democracy that blinded them to the harm that slavery, inequality in rights, protectionism, and monopoly privileges would wind up causing to their government and their principles.  She realized the founding fathers did not hate women, they just were blinded that not including the words women in the Constitution would lead to collateral deficits in the law affecting generations of women.  They were blinded because of their culture and society at the time did not allow them to see all facets of what their words might do 50, 100, 250 years into the future.

Do you think Ms. Ahern’s tweets will age well into the future as RBG ideas have?  Might the medium both used have something to do with this?  

I’m currently deeply concerned that Dr. Fauci has become modern medicine’s Joe MCCarthy.  His nonsense is destroying civil liberites in the name of pseudoscience.  It is being sold to the public under the guise of Big Pharma and vaccines to give it legitimacy.  

In 2020 America, many people speaking their “truth” on social media but they are really telling lies to their audience and the medium is giving them the ability to do so.  There is only the truth and it is not necessarily “yours”.  You are entitled to your opinion, but you’ve never been entitled to your own set of facts,  before social media arrived.  The medium allows you to cherry pick your data sets and this is fueled by your own cognitive biases and the network of people you surround yourself with.  Your circle of influence says a lot more about you than you want to admit.

This tells me this topic is current and important for you to understand if we are ever to trust one another.  It might be incredibly important for you trusting the scientific links I shared with you here in my past, present and future.    

I believe when you believe bad ideas or succumb to poor science it erodes trust.  It might even erode your trust in something that is true and give way to false beliefs.

When I read the tweet, I immediately thought about the video above and how bad science is now created for propaganda to sell things to people that they really don’t need for health. In fact, if they buy it, it might make them unhealthy. Then I thought about social media and bad ideas and how they spread. Is this why so much of what we believe is FALSE.

We’ve all heard the cliche, the medium is the message. If this is true today, what is our mediums doing to our messaging?

Does the medium of communication contain the seed of destruction for the message, ideas, or information?

Where did the cliche come from?  When it comes to understanding new media, one of the best to learn from is Marshall McLuhan. He was a Canadian born in 1911 and he died in 1980, McLuhan had no opportunity to experience the Web the way we know it today, but that didn’t stop him from exerting a huge influence on it.

It was McLuhan who first spoke about technology and communication having the ability to create a “global village.” As an early educator and pioneer of the study of communication and its evolution over time, McLuhan introduced a lot of observations about the impact of new forms of expression and media. Most notably, McLuhan’s expression “The medium is the message” has had a resounding impact not just on Web design but on mass media in general.

The video above shows you how a new medium has been created to sell things to people they do not need.  That is the point of predatory journals.  It gives cover to bad science and bad scientists.  You, my audience need to fully understand the implications of this new medium so you vet your experts and what they push and sell you and make sure they are not using predatory journals to push pseudoscientific ideas in your direction.  You might never know why their bullshit appears genuine.  Here is an example of a “doctor” selling you, the public an idea that was created in a predatory journal as the video above showed.  Who is packing your parachute?

Now that you know that DEFCON 26 outed GcMAF in the video above, how will this temper how you see Dr. Dietrich Klinghadt’s advice on anything in the future? Did he dig deep enough for his tribe to uncovered truth or did he use predatory journals to create profit for himself? Will Ms. Ahern’s tweets give you confidence that her vision of the present and future is built on a strong foundation? Do you like the way she has used words since she is now an author? Has the medium really helped her?

See, outing bullshit and bullshitter’s has a deep purpose to someone on a journey to see the truth……….the medium we use and how we use has a deep message for our audience.

Since the early days of communication, humanity has been captivated by the methods it uses to convey and preserve information. How we communicate with each other defines who we are and constitutes so much of what makes a culture and an individual unique. 

What if our current use of social media is destroying our human identity and destroying truth so that we get further from the answers society really needs?    If the medium is the message, what is the medium telling you, my student Black Swan, today about how we think about our world?

When I read Ms. Ahern’s Tweet I immediately thought to myself, “maybe these people I should spend some time on and try to help?”   The sudden death of RBG really caused some chaos in the mind of Ms. Ahern.  RBG was a liberal thinker.  She was not progressive.  Progressives always seem to deal in hopes rather than in facts…….Ms. Ahern however, is very progressive in her thinking.  I do not even think she realizes that she is anti RBG in her thoughts, but I want you to think about that idea and see if I am right or wrong in telling it.

That is when i decided to pen this blog to teach my tribe that social media is harming truth, the truth’s in Nature’s recipes that guys like Dr. Fauci and Mark Zuckerburg are trying to hide from you.

Less than 24 hours ago I was banned on FB for telling people that the sun, via Vitamin D creation was a great therapeutic idea for COVID19.

I posted two articles from non predatory journals that support the use of the sun and Vitamin D as a preventative cure from COVID 19.  Then I got this:

I had my legs cut out from underneath me.  I was censored.  What did I do.  I fought back using the medium and the pen as my message to my tribe.

If you feel as if your legs have been cut from underneath you, as Ms. Ahern did above in her tweet, instead of wallowing in despair get back up on your feet and touch the door that you feel has closed to you. If a door you value has closed for any reason, you should spend or waste any more time staring at it.  Ms. Ahern is a budding author.  She better think about the path she is on now.  

When you write to help others never compromise to someone else’s standards.  You have two choices in your life.  Live by your own choices or you’ll be forced to live by someone else’s.  Better to write for yourself and your own standards and have no public, than to write for the public and have no self.  The world is not ready for some folks when they show up, but that shouldn’t stop anyone from trying to help mankind.  Some things in life just can’t be bartered over or placed on the sale rack – and your self-worth is at the top of the list.

Be at peace and look for an open door. It’ll be there. Life is not lived through just one door. Then, walk through that new door it into the next phase of your life. A closed door is nothing but a new opportunity for new life experiences. One that might be greater than the life you knew in the old room, with the locked door tied to it.   RBG did it and so can you.   

Above Erin Schaff a NYT photographer, take a picture where you see conservative women, who support Judge Amy Coney Barrett’s nomination to the Supreme Court, pray while touching the doors of the Court as progressive leftist Jacquelyn Booth lies, crying on the ground, mourning the death of Justice Ruth Bader Ginsburg.

What was Ms. Schaff trying to convey to her Twitter audience if the medium is the message?

When the doors begin to close, the mind should begin to open.

Are you victim of life, or are you capable of overcoming your fears by thinking fiercely well?

How smart are you?

Do you find logic in false ideas?

Why does this happen to you?

Faced with a choice between changing one’s mind and proving there is no need to do so, almost everyone gets busy with the proof. The most difficult subjects can be explained to the most slow-witted man if he has not formed any idea of them already; but the simplest thing cannot be made clear to the most intelligent man if he is firmly persuaded that he knows already, without a shadow of doubt, what is laid before him. Does being super wrong about something in the past negate a current idea that is fabulous?

What’s going on here? Why don’t facts change our minds under a technocracy? And why would someone continue to believe a false or inaccurate idea anyway? How do such behaviors serve us?

2020 has shown us all that humans need a reasonably accurate view of the world in order to survive. If your model of reality is wildly different from the actual world, then you struggle to take effective actions each day.

In my opinion, social media acts to destroy real truths by giving every user a perception of the tech companies algorithm which is built around their version of the truth. Their truth is design around separting you from your dollar just by slightly getting you to change your behavior because of what their algorithm does to your brain via a blue lit screen.

How do I use social media?  I train wolves to think.  Help me find some more of them.  Share this with them if you enjoyed this journey through my mind.  

CITES: 

In My Own Words, RBG.  https://www.amazon.com/gp/product/1501145258/ref=as_li_ss_tl?ie=UTF8&linkCode=sl1&tag=lfdigital-20&linkId=033f04d2ec535d134930c041ebc307be

Twitter feed of Ms. Ahern and Schaff

The movie: The Social Dilemma on Netflix.

Is nighttime and DAYTIME technology devices use to blame for the etiology of most diseases in humans? Yes, I believe it is today. WOW. That is a big statement, Uncle Jack. How and Why? Here is a recent slide from a presentation I gave to shock my audience below.

Melanopsin, like the cone photoreceptor, is a PHOTORECEPTOR TOO FOR BLUE LIGHT. ALL OPSINS in humans are bound to retinol, and when the photoreceptors are damaged it is because of the atomic changes in retinol when the weak covalent bound it broken by light out of the normal circadian cycle.

What is the take home? The blue light hazard associated with man made light or the light present in all laboratories globally today generates massive levels of mitochondrial ROS and oxidative stress occurs directly in the outer segments of photoreceptors after blue light irradiation leading to disease. The cites below show that this statement is not hyperbole. It is now PEER reviewed published reality.

If you want to know where melanoma begins read the last cite in listed below. Melanocytes sense blue light and regulate pigmentation through Opsin-3 = melanopsin.

It took 90 years for “medical science ” to rebut the claim that linoleic acid is essential in any human diet, a claim that has led to an incalculable mischief in terms of dietary advice and disease prevalence, In the last two centuries. How many decades will it take for the average physician or your physician to read those papers covering the nutrition debacle? How long will it take to change their advice or their practice of the healing arts?

I believe it might take several hundred years to get people to understand that blue light from man made devices is more deadly than any other stimulus man has created in the last 120 years because our focus in in nuclear DNA and not on the mitochondrial DNA mutations cause by blue light.

In 1998, we found melanopsin in the retina. In 2009 we found neuropsin in the skin and cornea. In 2014, we found melanopsin in the arterioles of the human body. This tells us all we are creatures of light who capture and transform the light of the sun into energy that cells use to create life and health.

In December 2017, we found melanopsin in the skin and subcutaneous fat of humans. This was huge news to those who understand leptin and that leptin the fat hormone is also found within the subcutaneous fat of MAN. The data is telling us why we have an obesity crisis and it has NOTHING to do with food or exercise but it has a lot to do with circadian arrhythmia of light in our eye and skin and subcutaneous fat mass.

The nighttime and daytime light environment has changed dramatically due to modern technology. Increased usage of mobile devices during ANYTIME OF THE DAY can disrupt your circadian clock. PEOPLE forget that the melanopsin receptor is regenerated DURING daytime!!!! So if you are around man-made blue light during the day you are still ruining your melanopsin photoreceptors. The intense light emitted from technology devices in screens has the potential to alter the timed release of factors within the eye, leading to chronic insults and susceptibility for visual damage. What does this mean to melanopsin photoreceptors?

I gave you my answer in the Vermont 2018 video.

Recent findings cited below to suggest a functional role for the circadian clock in mammalian cone photoreceptor development and provide evidence for a continuing role for thyroid hormone (TH) signaling in cone photoreceptor maintenance. These researchers have said their findings may be of relevance in OTHER tissues where human photoreceptors are as well, where the circadian clock could alter tissue function by directly regulating enzyme type 2 iodothyronine deiodinase (Dio2) expression and thus TH signaling.

THAT is WHAT the data I presented in VERMONT 2018 is all about. I hope you view the talk. It is well worth it to further your education. Once you realize and know where melanopsin is, and follow the damage in its wake, you begin to see where mitochondrial disease begins for the very first time in your life. It happens where clinicians least expect it and that is why they always miss it and the public cannot be helped via a prescription pad. That is where the data is now……..it is not in food/exercise choices, it is made in the light choices we make.

With this new information, researchers can begin to ask questions such as, “How else can we change the photoreceptors in humans using light evolution has never used? Are there other factors that can improve photoreceptor function and help extend their viability that we have failed to consider in science and industry? The BLACK SWAN among you now knows this answer. It should be as clear as the nose on your face, because this new data is telling you disease generation is not what your doctors were taught in medical school.  Your light choices form your medical destiny.  

CITES:

https://consultqd.clevelandclinic.org/circadian-rhythms-thyroid-hormone-and-vision-loss/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048889/

https://yelling-stop.blogspot.com/2020/09/fat-and-weight-gain-note-to-peter-and.html

https://www.sciencedirect.com/science/article/pii/S2212492619300892

 

• Mondini dysplasia can cause chronic tinnitus. This defect comes from a defect in the Fibonacci sequences during embryogenesis and can lead to defects in melanosis that can profoundly affect hearing and tinnitus generation in the dysplastic brain.
• The Fibonacci numbers form a sequence of numbers defined by a relationship mathematically.  What this means, in English, is that it is a sequence of numbers whose relationship is this: after the first two numbers, each proceeding number is the sum of the previous two numbers. For example 0, 1, 1, 2, 3, 5, 8, 13, 21, 34, 55, 89, 144, 233…..and so on. Quite simple, really.
• Fibonacci numbers are not purely artifact, they are also found in nature in an uncurling fern, the branching of trees, and leaflets of the pineapple. The Fibonacci sequence also describes the “golden spiral,” which is when a “golden rectangle” is subdivided in smaller and smaller golden rectangles —the result being a predictable spiral.
• Fibonacci numbers have an interesting property. When you divide one number in the sequence by the number preceding it, you are left with a number very close to 1.618. This number is called the “golden ratio,” and rectangle whose sides is equal to the golden ratio is known as a “golden rectangle.”
• One example of a biological structure in the mammalian body which is very close to a “golden spiral” is the cochlea.  You can see that spiral below in blue.

• The Mondini malformation and Mondini defect is an abnormality of the inner ear that is associated with sensorineural hearing loss and tinnitus. This deformity was first described in 1791 by Mondini after examining the inner ear of a deaf boy. The Mondini dysplasia describes a cochlea with incomplete partitioning and a reduced number of turns, an enlarged vestibular aqueduct, and a dilated vestibule. A normal cochlea has two and a half turns, a cochlea with Mondini dysplasia has one and a half turns; the basal turn being normally formed with a dilated or cystic apical turn to the cochlear. The hearing loss can deteriorate over time either gradually or in a step-wise fashion and it can lead to debilitating tinnitus as hearing is destroyed. Destroying the ear with deafness operations might actually make the tinnitus worse. Cochlea implants might be a better way to deal with dysplastic auditory cortex.

About one in five people experience tinnitus, the perception of a sound—often described as ringing—that isn’t really there. Tinnitus brain mapping has revealed just how different tinnitus is from normal representations of sounds in the brain.

Perhaps the most remarkable finding from the brain mapping experiments was that activity directly linked to tinnitus was very extensive and spanned a large proportion of the part of the brain that researchers measured from during brain surgery. This tells us that tinnitus is really not a peripheral disease but a sensory processing disorder.

Only a few groups in the world have the expertise and collaborative infrastructure to conduct these neurosurgical experiments. It is possible because patients who require invasive brain mapping in preparation for epilepsy surgery also volunteer to participate in research studies. The University of Iowa has the ability to do this because of their epilepsy program.

It is such a rarity that a person requiring invasive electrode monitoring for epilepsy also has tinnitus. Some people do not have epilepsy but have been found to have other neurovascular abnormalities that might the cause of the tinnitus.

Iowa’s epilepsy team puts a recording platform into the patient’s brain for clinical purposes and they can modify it without changing the risk of the surgery. This allows them to understand functions in the brain in a way that is impossible to do with any other approach.

Iowa researchers contrasted brain activity during periods when tinnitus was relatively stronger and weaker. They found the expected tinnitus-linked brain activity, but they report that the unusual activity extended far beyond circumscribed auditory cortical regions to encompass almost all of the auditory cortex, along with other parts of the brain.

The sheer amount of the brain across which the tinnitus network is present suggests that tinnitus may not simply ‘fill in the gap’ left by hearing damage, but also actively infiltrates beyond this into wider brain systems based on the findings of this paper below.

These new insights should help to inform treatments such as neurofeedback or optogenetic therapies, where patients learn to control their “brainwaves,” or electromagnetic brain stimulation.

A better understanding of the brain patterns associated with tinnitus may also help point toward new photobiomodulation approaches to treatment.

The team included the University of Iowa researchers Hiroyuki Oya, Gander, Sedley, and Howard and Christopher Kovach, Kirill Nourski, and Hiroto Kawasaki, as well as Timothy Griffiths at Newcastle University. The research was supported by grants from the National Institutes of Health and the Wellcome Trust and Medical Research Council in the U.K.

Tinnitus appears to be a sensory processing disorder whose causes are multiple but all lead to a sensory processing disorder in the thalamus and auditory cortex.  Mondini’s dysplasia is one of many things that cause this cortical dysfunction in the auditory part of the brain.

CITES:

https://www.cell.com/current-biology/fulltext/S0960-9822(15)00278-X

DO TINNITUS, PD, and AD all RELATE TO blue light and nnEMF via hypoxia?

In the human ear, there are melanocytes present in the hearing mechanism which are cells that form melanin. Melanin is a UV light-absorbing pigment that can be made from tyrosine or phenylalanine. You can see from the picture above that the action spectra of light from both aromatic amino acids is 220-300nm light which is deep in the UV range. This implies the light frequencies are somehow linked to how and what we hear. Tinnitus is a warning symptom that your nnEMF environment is sub-optimal. The question is for the inquiring mind, is why did evolution put this photochemical in our hearing apparatus?

Might melanin be how we tune into our environment first before sound affects us?

Remember light travels way faster than sound so from a physics standpoint using light for the afferent sensory reflex loop makes a lot of quantum mechanical sense. It just offends your doctor’s common sense. That is a good thing for a Black Swan. We ask questions few people do.

In this system, full-spectrum solar light is critical because it contains the 200-400 nm light tyrosine/phenylalanine that needs to create melanin. Melanocytes make melanin from aromatic amino acids (tyrosine) that all have hexagonal rings of carbon that absorb UV light from 220 nm to 300 nm. For this mechanism to tune properly, you first need AM balanced light in the visible spectrum that has no UV light present. The dose of the blue light present is stimulatory to the pituitary gland but this pro-growth stimulus is always protected and balanced by the 42% of IR-A present early in the AM. The next light that shows up diurnally in solar exposure is UV-A light in the AM. when it shows up varies based upon your latitude. This explains why tinnitus is rare inside the tropics where light is more stable. I expect this will change as people inside the tropics begins to use technology from the US. This will ruin their afferent reflex loops.

Melanosomes in the ear pay attention to UV light’s arrival by having melanin’s electrons become excited by the sun rays. To activate the system the ear pinna and external auditory canal need the full day spectrum solar light to develop naturally. This includes IR-A, UV-A, and UV-B based upon your latitude and altitude.

The human ear effectively “measures” the light radiation environment you allow via your choices and helps fine tune your hearing by reacting with the photon traps in tyrosine and phenylalanine with the formation of melanin as hearing protectors. If the radiation environment is disturbed (by man-made light), limited or no melanin is formed in the pinna or in the external auditory canal.

Without this initial stimulus, human hearing becomes affected and our hearing becomes susceptible to an improper energy transformation.

People forget that when light collides with melanin the electromagnetic wave becomes and electro-mechanical wave or an electromechanical wave called a phonon/soliton. What is the target of this phonon or soliton? Look at the picture below. Is there a pigmented vascular layer in the inner ear? Yes, there is. Why do we have light pigments in our cochlea? And why do we have melanin in our pinna and our ear canal? These are questions Black Swans ask themselves to understand why their hearing is altered.

Those phonons are targeting pigmented cells in the body of the cochlea by a process of chemiexcitation. If solar light is absent and man-made light dominant in your environment the transformation these light waves into mechanical-acoustic signals (phonons/solitons) is disturbed. This is how tinnitus begins quantum mechanically in my opinion. The afferent reflex arc is disrupted by nnEMF light waves sensed on the external ear and in our ear canals.

Melanin is a pigmented polymer with a known role in dermal solar protection. In vertebrates, melanogenesis has been reported in leukocyte population of cells suggesting a potential role in innate immunity. An altered innate immune response is one of the first things ENT surgeons should suspect in people with tinnitus but few do because they do not know about this link.

The presence of melanin in the inner ear was established more than a century ago, but the exact biological function of the pigment in the labyrinth has yet to be determined in medical textbooks. This is why tinnitus remains a mystery for docs and their patients afflicted with it.

Special attention should be drawn to the composition of melanin. Melanin is a biological reservoir for divalent ions like calcium and as an ion exchanger, as well as an intracellular buffering system for calcium. nnEMF alters the resonance frequency of this atom. nnEMF also alters voltage-gated channels that control calcium flow. This explains why melanin and nnEMF are likely linked to the symptom of tinnitus. It should be pointed out to the non learned that melanin is capable of binding ototoxic drugs. Finally, morphological responses of melanocytes happen when local disturbance of Ca++. Below you can see how calcium is quantized to the light that affects the afferent loop in this reflex.

One last link of Ca2+ release to another ear disease is Meniere’s disease which is often linked to tinnitus.  An altered level of melanin or an imbalance of its functioning can create an imbalanced Ca2+ homeostasis in the inner ear.   This has been demonstrated using  endolymphatic hydrops (EH) as an animal model for Meniere’s disease. These models have shown us that there is a  possibility of a receptor-mediated Ca2+ transport across the pigmented epithelial layer, especially the light cells, and the presence of a ‘chemical signal’ as an initiating modulating factor in the disturbance of Ca2+ homeostasis.  It appears light tunes the cochela using calcium as the electromechanical lever.  It is pointed out numerous times in the PEER reviewed literature that melanin is capable of binding calcium and may act as a buffering system in hearing and in balance.

Quantum mechanics rarely extends to molecular medicine. Recently, the pigment melanin was found to be susceptible to chemiexcitation, in which an electron is chemically excited to a high-energy molecular orbital. In invertebrates, chemiexcitation causes bioluminescence; in mammals, a higher-energy process involving melanin transfers energy to RNA and DNA and mtDNA without using photons.  This can create lethal and mutagenic cyclobutane pyrimidine dimers that can cause many diseases. This process is initiated by the free radicals NO and O2-. Their formation can be triggered by nnEMF light and/or inflammation. Several chronic diseases share two properties: inflammation generates these radicals across the tissue, and the diseased cells lie near melanin. I have said for 15 years that that nonquantized chemiexcitation may be an upstream event in numerous human diseases that lead to mitochondrial damage.

DNA AND mtDNA REPAIR IS NOT EQUIVALENT

Nuclear DNA repair of UV pyrimidine dimers in Chinese hamster ovary cells (CHO cells) is very selective with preferential repair of only sequences containing actively transcribed genomic regions. In essence, the literature over the last 30 years has shown very little repair mechanisms of these dimers in the entire mitochondrial genome of any animal tested.  Nuclear DNA repair mechanisms are quite rapid and very accurate.  Direct nuclear DNA action is likely not the mechanism that leads to disease.  Research has shown, even actively transcribed areas in mtDNA do not appear to be repaired in mitochondrial DNA. This data is in agreement with that previously reported in HeLa cells and in yeast  where a lack of repair of pyrimidine dimers in mitochondrial DNA was also observed.

The chemiexcitation path to diseases is a new quantum mechanical idea. It has long been known that photons of ultraviolet radiation from sunlight can be directly absorbed by DNA, where they excite DNA bases. If two excited pyrimidines (thymine or cytosine) are adjacent in RNA, DNA or mtDNA, a double bond forms automatically by the action of light. UV light can do this but it blue light is also quite capable of doing this as well.  When blue light creates ROS and RNS it opens thymine or cytosine to form two single bonds between the bases and makes a cyclobutane pyrimidine dimer (CPD); this [2+2] cycloaddition reaction can only happen if the bases are in an excited state by light.  Sunlight normally can lead to cell death via apoptosis.  It can also stimulate NK cells to take out the altered cell filled with mitochondrial disease and viral loads.  Alien light does not stimulate immunosurveillance in the same “quantized way” that sunlight does and this can lead to cancers or other mitochondrial disease.  This is often associated with co-morbid hypoxia in the cell.   Immunological surveillance is a monitoring process of the immune system to detect and destroy virally infected and neoplastically transformed cells in the body.  This is why altered melanosis is linked to both viral illness and cancers.

The CPD disrupts base pairing and distorts the DNA helix, leading to cell death or – when DNA replicates – a C→T mutation. Mutations in oncogenes and tumor suppressor genes are required for disease generation like cancer. Chemiexcitation instead excites the DNA bases long after light exposure has ended because of how melanin operates with light. In this situation, light radiation serves to activate enzymes that synthesize the radicals NO• and O2•−for hours afterward. These radicals form peroxynitrite, which oxidizes melanin or its monomer DHICA (5,6-dihydroxyindole-2-carboxylic acid) and allows ambient O2 to create a dioxetane on the melanin. The dioextane moiety, is a strained 4-atom ring containing –C–O–O–C–, is unusual in being able to release large amounts of energy in a single reaction, creating long-lived, high-energy, electronically excited triplet states (denoted by * below).

This triplet energy can transfer to RNA/DNA/mtDNA, resulting in a CPD without the involvement of photons. Thereafter, an unrepaired CPD would again result in mutations or cell death. The same radicals are formed during normal cellular inflammation from nnEMF damage, creates the same end product can be created by enzymes like horseradish peroxidase (HRP), prompting the idea that chemiexcitation can occur in internal organs leading to a myriad of diseases that today have no explanation of what causes them. This mechanism is likely why RF and microwave radiation damaged the ears and brains in people stationed in the Cuban embassy a couple of years ago when and Electromagnetic device was aimed at our emabassy to cause damage to US citizens.

Human mitochondria have their own DNA, which is double- stranded, circular and contains —16,569 base pairs. The mitochondrial genome has been sequenced in its entirety and consists of genes that code for 13 subunits of the respiratory chain complexes, 22 tRNAs and two rRNAs. Until recently, the only mitochondrial DNA defect that appeared to be of significance was that of a mutation in one of the mitochondrial ribosomal RNA genes which conferred chloramphenicol resistance. However, within the past 30 years defects in the mitochondrial genome have been described in a number of human diseases. The initial description by Holt et al. of deleted mitochondrial DNA in patients with mitochondrial diseases has been confirmed by  numerous studies which found that mitochondrial deletions occurred in > 90 % of cases with Kearns—Sayre syndrome. Additionally, mitochondrial point mutations have been associated with Leber’s hereditary optic neuropathy, Pearson’s syndrome, autism, T2D, and some cases of chronic progressive external ophthalmoplegia. Accumulations of mutations in mitochondrial DNA have also been reported in the brains of patients with Parkinsonism and Alzheimers disease. These findings suggest that mitochondrial DNA defects are of biological importance in modern medicine.  It makes you wonder why medicine keeps ignoring these links.

What does all this imply?  If you live at a high latitude, with poor sunlight, have too much nnEMF in your life that causes hypoxia, or you live in a large city with many people addicted to technology, you are at risk for hearing loss and tinnitus.  It also might be a precursor symptom to macula degeneration and neurodegeneration in the brain.  Anywhere melanin is located, chemiexcitation can cause mtDNA damage and cause a hum in your ears.

CITES:

Chemical excitation of electrons: A dark path to melanoma.Premi S, Brash DE.DNA Repair (Amst). 2016 Aug;44:169-177. doi: 10.1016/j.dnarep.2016.05.023. Epub 2016 Jun 1.PMID: 27262612

• UV-induced Melanin Chemiexcitation: A New Mode of Melanoma Pathogenesis.Brash DE.Toxicol Pathol. 2016 Jun;44(4):552-4. doi: 10.1177/0192623316632072. Epub 2016 Mar 7.PMID: 26951162
• Role of Melanin Chemiexcitation in Melanoma Progression and Drug Resistance.Premi S.Front Oncol. 2020 Aug 6;10:1305. doi: 10.3389/fonc.2020.01305. eCollection 2020.PMID: 32850409
• Photochemistry. Chemiexcitation of melanin derivatives induces DNA photoproducts long after UV exposure.Premi S, Wallisch S, Mano CM, Weiner AB, Bacchiocchi A, Wakamatsu K, Bechara EJ, Halaban R, Douki T, Brash DE.Science. 2015 Feb 20;347(6224):842-7. doi: 10.1126/science.1256022.PMID: 25700512
• Unanticipated role of melanin in causing carcinogenic cyclobutane pyrimidine dimmers.Premi S, Brash DE.Mol Cell Oncol. 2015 Jun 23;3(1):e1033588. doi: 10.1080/23723556.2015.1033588. eCollection 2016 Jan.PMID: 27308551

Do you know the purpose of the unusual construction of the mitochondrial membranes? Did you know that the inner mitochondrial membrane is the ONLY membrane in humans that is DEVOID of DHA? Do you know why the membranes in the mitochondria are built by Nature to be extremely hydrophobic? Do you know that these membranes can carry voltages close to 30 million volts because of this build-out? Do you know that one of these membranes actually makes water from food? Did you know that the atomic construction of this water also has to be specifically depleted of a certain isotope? Do you know why all these things exist in your mitochondria?

The answer might shock you. Uncle Jack is going to tell you that all these things occurred 650 million years ago to suspend the laws of physics to allow nature to do things not even gods could fathom. Nature figured out how to use nanoscale spaces to suspend physics to build the possibility of life.

Did you know when a thin layer of water is squeezed between two hydrophobic surfaces, the laws of classical physics break down? Well, I have been teaching my members this since my epic April 2016 webinar on what life really is up too. Now you have more data I am on the right track and the paradigm and all my critics remain myopic.

The take-home is this: PHYSICS IS THE SCIENCE OF PROBABILITIES. BIOLOGY IS THE STORY OF THE IMPROBABLE AND BIOLOGY CAN ONLY MAKE SENSE FROM THE PERSPECTIVE THAT THE LIVING STATE IS ONLY PROBABLE USING REACTIONS WHICH ARE STATISTICALLY IMPROBABLE.

So Nature built cells to have the ability to suspend what we should expect to give us the most improbable answer why life really exists and happens. She figured out how to suspend her own laws using things she built. How is that for counterintuitive?

That is why I teach Black Swans how to think. Black Swans are rare. They go deeper to find wisdom than others would. I call these people Black Swan mitochondriacs. Humans that actually take the time, to read, research, and read about science that on the surface seems superfluous, but is foundational to our health on the submolecular quantum level.

Nature does not employ any “balanced protocol” in her usage. She is all about unbalancing the scales to favor the tasks that cells need to accomplish. NEVER FORGET IT.

And anyone who says otherwise will have to explain this new finding.

People who have open minds to accept new data that blows your paradigm of beliefs apart.

Why do living things prefer the lighter isotope of hydrogen than the heavier version of hydrogen called deuterium?

Heavier things make quantum mechanics “less probable”.

In the early 1980s, researchers first noted an unexpected effect when two hydrophobic surfaces were slowly brought together in water. At some point, the two surfaces would suddenly jump into contact—like two magnets being brought together.  No one knew why or how it happened.

Part of this research challenge was to realize that the hydrophobic interaction is unique to liquid water.   No other solvents are capable of this effect.  Living things are most made of water.    Your colony of mitochondria make water.

The smaller an object/atom is, the less strictly it is governed by the laws of classical physics, and the more it is subject to quantum effects. A tiny hydrogen atom is a quantum object—sometimes behaving like a particle, sometimes more like a wave. Deuterium, twice as heavy as hydrogen, is less subject to quantum effects. The consequence is that D2O is less destabilized than H2O when squeezed between two hydrophobic surfaces and the hydrogen bonds between water molecules get broken. It turns out life wants to shapeshift water’s hydrogen bonds with light to create the magic that life uses.

When mitochondria are non optimal they are making less water and they become hypoxic. This changes the delta psi or the electric charge on its membranes and this lowers the redox potential. We can see this effect via our endogenous glutathione levels on testing. This lowers the probability of these quantum nuclear effects in water making illness more likely over health.

This tells us that this effect is important in creating the living state.  This new research work shows how quantum nuclear effects in water become substantial on the nanoscale.  that is the scale your cells operate in.

Nature is capable of a lot more than we believe.

CITES:

“Nuclear Quantum Effects in Hydrophobic Nanoconfinement” by Buddha Ratna Shrestha, Sreekiran Pillai, Adriano Santana, Stephen H. Donaldson Jr., Tod A. Pascal and Himanshu Mishra, 31 July 2019, Journal of Physical Chemistry Letters.
DOI: 10.1021/acs.jpclett.9b01835

 

 

 

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 to have 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.