Category: Medicine

bookmark_borderCOVID: The Natural Immunity Myth

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by Daniel Brouse
August 30, 2021

To date, there is zero (0) evidence that contracting the original strain of COVID gives you any immunity to re-infection — natural immunity. On the other hand, there are a multitude of examples of re-infection.

Natural immunity to the original strain lasts on average from 60 days to 6 months; however, there does not appear to be any natural immunity to the variants.

In India’s recent wave, 1 in 4 Delta cases were re-infections. “Antibodies against Sars-CoV-2 — the virus that causes Covid-19 — were found in about 27% of the 91 participants at a time when the second wave was raging in the country, researchers at the Institute of Genomics and Integrative Biology, National Centre for Disease Control and the Cambridge University, said.” — Hindustan Times

“During the Novavax vaccine trials in South Africa, the study found an overall primary efficacy of 49.4% in 4,400 participants, meaning about half of the patients vaccinated and later infected did not experience symptoms. Genomic analyses revealed that about a third of the 4,400 were previously positive for infection, meaning the South African variant was then and is now capable of reinfection, evading neutralizing antibodies in a similar capacity to the Brazilian variant.”

“The study also showed that prior infection with an earlier version of the virus did not reduce the risk of COVID-19 caused by the South African variant among people who got placebo shots.” — Reuters

Another variant (C.1.2) related to the original South Africa variant (C.1) was discovered in South Africa, China, the Democratic Republic of the Congo, Mauritius, England, New Zealand, Portugal and Switzerland. A study by the National Institute for Communicable Diseases (NICD) and the KwaZulu-Natal Research Innovation and Sequencing Platform (KRISP) in South Africa found the variant could be more transmissible and evade protection provided by vaccines and prior infection.

“Among Kentucky residents infected with SARS-CoV-2 in 2020, vaccination status of those reinfected during May–June 2021 was compared with that of residents who were not reinfected. In this case-control study, being unvaccinated was associated with 2.34 times the odds of reinfection compared with being fully vaccinated.” — CDC

“Our case series shows that reinfection with different strains is possible, and some cases may experience more severe infections with the second episode. The findings also suggest that COVID-19 may continue to circulate even after achieving herd immunity through natural infection or vaccination, suggesting the need for longer-term transmission mitigation efforts.” — Journal of Investigative Medicine

Vaccines do not appear to be much more effective against the Delta variant than natural immunity through infection. The increase of breakthrough cases has been increasing in lock-step with the increase spread of the Delta variant. “Fewer than 10% of new coronavirus infections occurred in fully vaccinated people in the weeks before June, but the rate increased this summer. In the first four weeks of August, roughly 30% of infections were in fully vaccinated individuals.” — The Star Tribune

A study by the CDC found vaccine efficacy dropped from roughly 90% to 66% as the Delta variant emerged. “This report updates vaccine effectiveness (VE) estimates including all COVID-19 vaccines available through August 14, 2021, and examines whether VE differs for adults with increasing time since completion of all recommended vaccine doses.” — CDC

Another CDC study that compared natural immunity to vaccination has found — “Among COVID-19–like illness hospitalizations among adults aged ≥18 years whose previous infection or vaccination occurred 90–179 days earlier, the adjusted odds of laboratory-confirmed COVID-19 among unvaccinated adults with previous SARS-CoV-2 infection were 5.49-fold higher than the odds among fully vaccinated recipients of an mRNA COVID-19 vaccine who had no previous documented infection.”

CONCLUSION PART I
There is a need for longer-term transmission mitigation efforts. Because reinfection is likely, vaccines efficacy is not high enough, and new variants are emerging, herd immunity is not achievable. Humans can not learn to live with the virus. Mitigation efforts must be made to stop community spread.

CONCLUSION PART II
COVID causes an immune dysfunction. When a person become infected, the SARS-CoV-2 virus alters your genes in order to infect you. “We identified EP300, MOV10, RELA, and TRIM25 as top candidates, and more than 60 additional proteins involved in the epigenetic response during viral infection that has therapeutic potential.” — Nature

When a person recovers from the virus, they are left with multiple gene alterations to there immune system. It is impossible for natural immunity to be feasible in an individual with an immune system that is compromised by a COVID-19 infection.

COVID survivors are left with a severe NAD+ deficiency, and an upregulation of IDO (which suppresses your T and NK cells.) Short term this makes your immune system dysfunctional. This means your antibodies can’t function properly and have little to no memory. Long term it makes you more likely to have heart, blood, respiratory, and neurological disorders. You are at high risk of developing dementia. In addition, you have reduced P53 genes (tumor suppression genes) putting you at higher risk of cancer. — The Membrane Domain

I strongly advise against contracting COVID.

OMICRON UPDATE
December 4, 2021

A study out of South Africa, “Increased risk of SARS-CoV-2 reinfection associated with emergence of the Omicron variant in South Africa,” found that individuals who recently recovered from the Delta variant were afforded little to no protection from the Omicron variant. “Population-level evidence suggests that the Omicron variant is associated with substantial ability to evade immunity from prior infection. This finding has important implications for public health planning, particularly in countries like South Africa with high rates of immunity from prior infection.”

As stated above, everybody is advised to:
* speak to your doctor
* get vaccinated
* wear an N95 mask
* stay socially distanced

UPDATE June 2022: No Immune Boost From Omicron
“If you were infected during the first wave, then you can’t boost your immune response if you have an Omicron infection,” said Prof Rosemary Boyton, of Imperial College London, a co-author of the study. “When Omicron started flying around the country, people kept saying that’s OK, that will improve people’s immunity,” said Boyton. “What we’re saying is it’s not a good booster of immunity.”

“It’s actually worse than that, because the adaptations that the spike [protein] has now are actually inducing a kind of regulation or shutdown of immune response,” Prof Danny Altmann, another author of the study, adding that while the study looked at responses to the BA.1, similar findings were likely for other subvariants of Omicron.

No Immunity Boost From Infection — view the PDF

COVID in Your Genes

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderLong-COVID: What We Know About Long Haulers Syndrome

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COVID=19
by Daniel Brouse
August 25, 2021
help@membrane.com

Post Acute Covid Syndrome 19 (PACS19), long-COVID, and Long Haulers Syndrome are names for the condition that an individual has after recovering from the SARS-CoV-2 virus. Long-COVID is actually a combination of several conditions and syndromes including changes to your genetics, an accelerant to aging, and the persistence of the virus in multiple organs for long periods of time.

The CDC Panel Report Long COVID Panel Survey found:

* 81% of adults with ongoing symptoms of COVID lasting three months or longer — or four out of five adults — are experiencing limitations in their daily activities compared to before they had the virus. (Economic implications include work force participation and long-term health care costs.)

* Young adults between ages 18 and 29 had the highest share of people currently with long COVID who have trouble performing daily tasks, at 86.3%. What will the long-term costs and quality of life be when these people are in their 50’s,60’s, and if they get to live into their 70’s?

There are over 60 proteins involved in the epigenetic response to COVID. So far out of these 60 proteins, three long-COVID epigenetic syndromes have been identified. There are likely many more. (The epigenetic changes are in addition to the organ damage caused by the virus.)

COVID-19 also causes other long term damage that we are still discovering.

Vaccines Help Prevent Secondary Complications
A study shows you are less likely to develop long-COVID Myocardial Infarction and Ischemic Stroke after a COVID-19 Infection if you ARE VACCINATED. Many people may not even know that COVID causes an increased risk of thrombosis. Vaccines can prevent secondary complications.

Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection (Vaccines Help Prevent Long-COVID Complications)

Rogue Antibodies
Autoantibodies are antibodies (immune proteins) that mistakenly attack a person’s own healthy tissues and organs. A study published in Nature found “rogue antibodies involved in almost one-fifth of COVID deaths. The self-targeting antibodies attack type 1 interferons that play a key role in fighting infection. Antibodies that turn against elements of our own immune defences are a key driver of severe illness and death following SARS-CoV-2 infection in some people, according to a large international study. These rogue antibodies, known as autoantibodies, are also present in a small proportion of healthy, uninfected individuals — and their prevalence increases with age, which may help to explain why elderly people are at higher risk of severe COVID-19.”

Up to three percent of the population already has faulty genes that create these autoantibodies. Of those between the ages of 18 and 69, 0.18% had existing autoantibodies against type 1 interferon. “Autoantibodies were present in around 1.1% of 70- to 79-year-olds, and 3.4% of those over the age of 80.”

A follow up study, “New-onset IgG autoantibodies in hospitalized patients with COVID-19,” found “Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection, is associated with many different clinical features that are commonly found in autoimmune diseases, including arthralgias, myalgias, fatigue, sicca, and rashes. Less common manifestations of autoimmunity have also been observed in COVID-19 patients, including thrombosis, myositis, myocarditis, arthritis, encephalitis, and vasculitis. These clinical observations, and the increasing proportion of “recovered” patients with persistent post-COVID-19 symptoms (so-called “long haulers”, or “long COVID”) suggest that inflammation in response to SARS-CoV-2 infection promotes tissue damage in the acute phase and potentially some of the long-term sequelae. A subset of autoantibodies targeting traditional autoantigens or cytokines develop de novo following SARS-CoV-2 infection.”

“The team also found that individuals with genetic mutations that disrupt the activity of type 1 interferons are at higher risk of life-threatening disease” suggesting COVID causes changes to the genes resulting in the creation of rogue autoantibodies.

In a study of healthcare workers, all had persistent autoantibodies, including ones that can cause chronic inflammation and injury of the joints, skin and nervous system. “We would not normally expect to see such a diverse array of autoantibodies elevated in these individuals or stay elevated for as long six months after full clinical recovery,” said Susan Cheng of the Cedars-Sinai Smidt Heart Institute in Los Angeles. (As reported in Paradoxical sex-specific patterns of autoantibody response to SARS-CoV-2 infection)

“We don’t yet know how much longer, beyond six months, the antibodies will stay elevated and/or lead to any important clinical symptoms,” Cheng said. “It will be essential to monitor individuals moving forward.” The team is investigating autoantibody elevations and their relationship to persistent symptoms in people with long-COVID.

NAD+ Deficiency
COVID both increases the breakdown of NAD+ and decreases the production of NAD+. “NAD regulates the inflammatory response in immune and non-immune cells through Sirtuins. Epigenetic regulation of histones and non-histone proteins is induced by sirtuins and is essential for the development, reprogramming, and differentiation of the immune system and its related pathologies. A deregulation of the NAD+ levels has been associated with metabolic diseases and aging-related diseases, including neurodegeneration, defective immune responses, and cancer.” — NAD-immune-system

The NAD+ deficiency results in a compromised immune system. The body can not properly metabolize vitamins nor mount a proper immune response. The NAD+ deficiency also resembles an autoimmune disease where the immune system appears to be attacking a healthy body. Without NAD+ regulating the immune system, the immune response becomes dysfunctional.

Though there is no cure for the NAD+ Deficiency Syndrome (CISP — COVID-19 Induced Secondary Pellagra), the symptoms can be treated with Niacin (Nicotinic Acid).

Upregulation of IDO
Indoleamine 2,3-dioxygenase (IDO) is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.

Memory T cells are crucial for the immune system to remember how to fight pathogens. IDO is also related to the viscosity of body fluids and membrane function. Brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears are some of the symptoms associated with epigenetic changes in the upregulation of Indoleamine 2,3-dioxygenase.

Dr. Ade Wentzel said, “The epigenetic upregulation of IDO will determine the amount of quinolinic acid. Quinolinic acid comes from the kynurenine pathway. If the viscosity of the whole middle ear is increased then the ability to equalize will be less… same as having a cold. So, the ear isn’t equalizing correctly on increasing pressure. The same as when you land in a plane. If the viscosity in the semicircular canals is increased, the otoliths may well be lagging causing the vertigo. The otoliths usually “Float” in the semicircular canal and trigger tiny sensory hairs that allow you to detect position.”

Coronavirus Transforms Pancreas Cell Function
When COVID infects cells, it impairs cell activity and can also change their function. When insulin-producing beta cells in the pancreas become infected with the virus, they produce much less insulin than usual, and also start to produce glucose and digestive enzymes. “We call this a change of cell fate,” said study leader Dr. Shuibing Chen, who described the work in a presentation at the annual meeting of the European Association for the Study of Diabetes.

It is not clear whether the changes are long-lasting, or if they might be reversible, the researchers reported in Cell Metabolism, “SARS-CoV-2 infection induces beta cell transdifferentiation“. “Single-cell RNA sequencing and immunostaining from ex vivo infections confirmed that multiple types of pancreatic islet cells were susceptible to SARS-CoV-2, eliciting a cellular stress response and the induction of chemokines. Upon SARS-CoV-2 infection, beta cells showed a lower expression of insulin and a higher expression of alpha and acinar cell markers, including glucagon and trypsin1, respectively, suggesting cellular transdifferentiation. Trajectory analysis indicated that SARS-CoV-2 induced eIF2-pathway-mediated beta cell transdifferentiation, a phenotype that could be reversed with trans-integrated stress response inhibitor (trans-ISRIB). Altogether, this study demonstrates an example of SARS-CoV-2 infection causing cell fate change, which provides further insight into the pathomechanisms of COVID-19.”

ALSO SEE: COVID: Insulin Reduction, Diabetes, High Cholesterol, Heart Disease and Stroke

Increased Risk of Cancer
In the case of cancer and tumor suppression, COVID chooses people that have reduced P53 (the tumor suppression gene.) It is also possible that COVID further reduces functional P53 genes. “Mutations in p53 are found in most tumor types, and so contribute to the complex network of molecular events leading to tumor formation.” — The p53 tumor suppressor protein

COVID also suppresses NK cells. “A type of immune cell that has granules (small particles) with enzymes that can kill tumor cells or cells infected with a virus. A natural killer cell is a type of white blood cell. Also called NK cell and NK-LGL.” — Natural Killer Cell

A study “Cancer Prevention with Resistant Starch” (conducted over the last 30 years) shows that resistant starch reduces your risk of cancer. The resistant starches produce good bacteria that reduces a type of acid that promotes changes to your DNA. The changes to your DNA increase the risk of many types of cancer. The discovery may also explain in part why COVID increases your risk of cancer. COVID is known to destroy good gut bacteria.

Permanent Organ Damage

“Dr Betty Raman, from the University of Oxford and one of the lead investigators on the study, says it is clear that those living with long-COVID symptoms are more likely to have experienced some organ damage.”

The biggest impact was seen on the lungs, where MRI scans were 14 times more likely to show abnormalities. Scans were also three times more likely to show abnormalities in the brain, and twice as likely in the kidneys, among people who had severe COVID.

The article Multiorgan MRI findings after hospitalisation with COVID-19 in the UK (C-MORE): a prospective, multicentre, observational cohort study was published September 22, 2023 in The Lancet Respiratory Medicine.

After hospitalisation for COVID-19, people are at risk of multiorgan abnormalities in the medium term. Our findings emphasise the need for proactive multidisciplinary care pathways, with the potential for imaging to guide surveillance frequency and therapeutic stratification.

ABOUT LONG-COVID
Long-standing multiorgan impairment following SARS-CoV-2 infection has been a major concern for individuals recovering from severe disease and is thought to be caused by a multitude of factors, including direct viral cytotoxicity, chronic inflammation, ischaemic injury, acute reactivation of other viruses, metabolic derangements, and acute treatment effects (especially invasive ventilation). Numerous reports of delayed organ complications such as myocarditis, stroke, and pulmonary emboli have led to speculations that the multiorgan dysfunction caused by COVID-19 might be responsible for impaired recovery and ongoing symptoms in individuals, a condition referred to as long COVID.

 

Long COVID Update:3 Years of Living With It

COVID-19 Chronic Conditions

COVID in Your Genes

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID Vaccine Breakthrough Cases

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by Daniel Brouse
August 23, 2021
help@membrane.com

Q: Why are there so many breakthrough cases of COVID in the vaccinated?

A: There are several reasons why there are breakthrough cases with any vaccine; however, COVID is different. Many of the vaccinated people getting COVID already had COVID prior to being vaccinated. This is the second time they have contracted the virus.

Once you have had COVID, your immune system is compromised. You should consider yourself immune compromised. The vaccine will not fully compensate for that fact. COVID damages your immune system. The virus makes your antibodies dysfunctional. The virus suppresses your memory T cells. The virus does a lot more to thwart an immune response. So though you may have the antibodies, maybe even lots and lots of antibodies, you’ve got Nobody’s At Home Syndrome. There is little to no immune response regulation nor coordination. This is also why natural immunity through infection is impossible. COVID erases the memory from your memory cells, so to speak. It can’t even remember itself.

Q: Is this a hallmark of the virus? I mean is this finding in all post COVID cases?

A: Yes. Severity of illness does not appear to be a factor (mild cases to severe all exhibit similar compromises to the immune system.) The exception is asymptomatic cases. We still don’t know about asymptomatic cases. The evidence is pointing to all cases that progress past the nasal passage result in immunocompromised individuals. There also is a small percentage (1 in 100,000) of people that appear to evade impact.

The scientific community is looking for ways to cure the problems. So far, there is only some success in treating the symptoms. There is nothing else to really compare to long-COVID. A similar condition happens to some measles survivors that bares a slight resemblance in T cell response, but it is not same. “Measles induces immune suppression through a process called immune amnesia. Studies in non-human primates revealed that MV actually replaces the old memory cells of its host with new, MV-specific lymphocytes. As a result, the patient emerges with both a strong MV-specific immunity and an increased vulnerability to all other pathogens.” COVID appears to use a different process that involves T cell suppression. There is also some similarity to HIV. “HIV attacks a specific type of immune system cell in the body. It’s known as the CD4 helper cell or T cell. When HIV destroys this cell, it becomes harder for the body to fight off other infections.” Again, COVID appears to use a different mechanism to suppress T cells.

Q: What do we know about the immune system post-COVID?

A: We know at least two important pieces of the puzzle:
1) The SARS-CoV-2 causes gene expressions in the host that result in dysfunctional NAD+. The virus makes it harder for the body to create NAD+ and also increases the breakdown in NAD+. “NAD regulates the inflammatory response in immune and non-immune cells through Sirtuins. Epigenetic regulation of histones and non-histone proteins is induced by sirtuins and is essential for the development, reprogramming, and differentiation of the immune system and its related pathologies. A deregulation of the NAD+ levels has been associated with metabolic diseases and aging-related diseases, including neurodegeneration, defective immune responses, and cancer.” — NAD-immune-system

2) The SARS-CoV-2 causes gene expressions in the host that result in upregulation of IDO (Indoleamine-2,3-dioxygenase). “IDO is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.’ (Wikipedia)

Q: How long do these gene expressions (epigenetics) last? How long does long haulers syndrome last?

A: We don’t know how long post-COVID cases will suffer with a compromised immune system. Long-COVID patients from January of 2020 are still immune compromised. It is possible the genetic changes will never revert.

COVID in Your Genes

COVID-19 Delta Variant and Vaccines

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID-19 Delta Variant and Vaccines

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COVID
By Daniel Brouse

What do we know about the Delta variant and vaccines?

OVERVIEW
The efficacy of mRna vaccines is about 79% against contracting the Delta variant. Non-mRna vaccines are between 40-60% effective against Delta. Vaccines lose efficacy at about 3%/month after six months of being fully vaccinated. Vaccines appear to help contain the Delta variant to the nasal passage. You are less likely to develop the epigenetic changes to your genes (long-COVID). Previous infection of COVID offers no protection to the Delta variant. Get vaccinated.

THE BAD NEWS
The delta variant is much more contagious than any other COVID strain. Vaccines also appear to be less effective at preventing infection from the Delta variant. On July 30, 2021, the Delta variant was much more predominant in Louisiana than in Pennsylvania. In Louisiana, 15% of the deaths were in vaccinated individuals. In Pennsylvania, 1% of the deaths were in vaccinated individuals.

Recent studies also revealed that vaccinated people can transmit the virus both asymptomatically and symptomatically.

THE GOOD NEWS
The vaccines are still tremendously effective at preventing infection, hospitalization and death from Delta.

Vaccinated individuals that get infected with Delta overwhelmingly stop the virus in their nasal passage. The virus never infects the lungs nor spreads to other systems causing blood clots or other life threatening conditions.

Since Delta never reaches the lungs and other organs, vaccinated people that test positive for COVID are unlikely to develop long-COVID (Long Haulers Syndrome). Long-COVID is caused by the coronavirus making epigenetic and genetic changes to your genes. COVID partially disables the immune system. Some of the dismantling is temporary lasting only a few days. Some of the dismantling is chronic and may last a lifetime.

The most common long term side-effect from COVID-19 are:
* the disruption of the body’s ability to produce and retain NAD+. Without NAD+ your immune system can not metabolize most vitamins, can not regulate body temperature, nor properly activate an immune response. Lack of NAD+ will cause your body to hi-jack tryptophan and cause all sorts-of mental and neurological disorders. Lack of NAD+ has been associated with over one hundred post-COVID ailments.
* upregulation of Indoleamine 2,3-dioxygenase (IDO). “IDO is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.’

In the vast majority of cases, vaccinated individuals do not suffer from alterations to the genes. Vaccination almost always prevents Delta from developing into long-COVID’s Long Haulers Syndrome.

PROTECT YOUR GENES FROM THE VIRUS
GET VACCINATED
WEAR A MEDICAL GRADE MASK (to prevent the virus from getting in your nasal passage in the first place)
TAKE A NIACIN SUPPLEMENT
AVOID ANTI-VAXXERS LIKE THE PLAGUE

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderLong-COVID and Environmental Aggravators

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by Daniel Brouse
help@membrane.com

Exercise aggravates long-COVID symptoms. COVID causes changes to your genes making it harder to create NAD+ and quicker to consume NAD+. Normally, exercise helps boost your NAD+. Not with long-COVID. The inflammation caused by exercise, anxiety, or exertion causes a rapid depletion of NAD+ aggravating long-COVID symptoms and perpetuating the downward cycle in NAD+ levels. So, Long Haulers should limit their activity until their NAD+ deficiency is under control.

What other factors can impact the severity of your long-COVID symptoms? We know anything that depletes NAD+ will cause problems. Aging, Hypertension, Obesity, Type 2 Diabetes, and other ailments result in suboptimal NAD+. But, what about your environment?

We know long term exposure to air pollution increases the risk of death from COVID-19 by 20 times. Another reason why wearing a mask in the out-of-doors is a good idea. Completely avoid outside exposure on air quality alert days.

I have been conducting research and development on two other environmental factors — elevation and temperature.

ELEVATION I — Change in Atmospheric Pressure
Elevation is the number of feet above sea level on which you stand. The bio-hacker experiment I’ve been conducting takes me from 400 feet above sea level to 1,400 feet above sea level. The more rapid the change from higher elevations to lower elevation, then the worse my long-COVID symptoms. All systems feel an impact; however, the middle ear takes the brunt of the punishment. Brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears are all amplified in their severity. I just did a 24 hour experiment and am beginning to think it has to do with pressure. Perhaps O2 (oxygen in the blood) as well, but more to do with “atmospheric pressure and sea level.” The symptoms seem to lag behind the increase in pressure.

Dr. Ade Wentzel said, “The epigenetic upregulation of IDO will determine the amount of quinolinic acid. Quinolinic acid comes from the kynurenine pathway. If the viscosity of the whole middle ear is increased then the ability to equalize will be less… same as having a cold. So, the ear isn’t equalizing correctly on increasing pressure. The same as when you land in a plane. If the viscosity in the semicircular canals is increased, the otoliths may well be lagging causing the vertigo. The otoliths usually “Float” in the semicircular canal and trigger tiny sensory hairs that allow you to detect position.”

“IDO (Indoleamine 2,3-dioxygenase) is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.’ (Wikipedia)

It is possible that changes in the weather that cause changes in atmospheric pressure (Lows and Highs) may result in the same problems. This happened to me with weather systems over the weekend (August 22, 2021.) A very low pressure system (hurricane Henri) passed by followed by a high pressure system. The following 2 days I suffered from brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears.

ELEVATION II — Oxygen Desaturation
People that go to higher elevations — above 4,900 feet — start to have more problems with High Altitude Oxygenation. “High altitudes can cause low oxygen saturation levels or desaturation of an individual’s blood.” Changing elevations at higher than 4,900 feet might cause both oxygen desaturation and atmospheric pressure problems.

COVID causes a decrease in the “rate of oxygen uptake into the lung to the oxygen gradient between the capillary blood and the alveoli.” Dr. Ade Wentzel said, “We know that the Lung Diffusion co-efficient is increased [by optimizing NAD+ levels].”

TEMPERATURE
The sweet spot is between 50-70 degrees Fahrenheit. The further below 50 degrees the more severe the symptoms. Lower temperatures appear to be a linear relationship. On the other hand, temperatures above 70 degrees appear to have an exponential relationship. That is to say, if 80 degrees causes symptoms to be twice as bad, 90 degrees causes symptoms to be four times as severe.

CONCLUSION
Mountain hiking in 90 degree temperatures (exercise at higher elevations in the heat) causes unnecessary stress on your system and dramatically increases your chances of a negative outcome.

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderPost-Acute COVID-19 — COVID Long Haulers Syndrome

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Guy A. Richards1, Adrian Wentzel2, Robert Miller

Post-Acute COVID-19 Sequelae
Post-Acute COVID-19 Sequelae


 

COVID-19: NAD+ deficiency may predispose the aged, obese and type2 diabetics to mortality through its effect on SIRT1 activity Wentzel, Miller, Richards
COVID-19: NAD+ Deficiency by Wentzel, Miller, Richards (PDF)

Treatment of SARS-CoV-2 induced pneumonia with NAD+ in a mouse model Jiang, Deng, Ma, Pang, Hu, Qin, Xu
COVID-19 in Mice / NAD+ (PDF)

Post-Acute COVID-19 Sequelae

COVID Sequelae
COVID Sequelae
AIMMS seminar 23 June | Role of NAD+ in (long)Covid - Part 1: Prof. Guy Richards - Clinical perspective
AIMMS seminar 23 June | Role of NAD+ in (long)Covid – Part 1: Prof. Guy Richards – Clinical perspective

AIMMS seminar 23 June | Role of NAD+ in (long)Covid – Part 2: Dr. Ade Wentzel – Pathophysiology and Treatment of Long-Covid + Q&A

AIMMS seminar 23 June | Role of NAD+ in (long)Covid - Part 2: Dr. Ade Wentzel - Pathophysiology and Treatment of Long-Covid + Q&A
AIMMS seminar 23 June | Role of NAD+ in (long)Covid – Part 2: Dr. Ade Wentzel – Pathophysiology and Treatment of Long-Covid + Q&A

MORE ON COVID
The Vitamin Stack / Long Haulers Treatment

COVID-19 / SARS-CoV-2 / Novel Coronavirus

 

bookmark_borderCOVID in Your Genes

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by Daniel Brouse
email help@membrane.com
May 30, 2021

COVID gets into your genes and makes alterations. Anybody that has “Long Haulers” (Post Acute COVID-19 Syndrome) can tell you about some of the resulting symptoms. COVID-19 Induced Secondary Pellagra (CISP) is one of the outcomes. CISP occurs when COVID changes your genome to chronically increase the breakdown of NAD+ and simultaneously decrease the production of NAD+ (nicotinamide adenine dinucleotide). NAD+ is in every cell and is involved in cell creation, maintenance, metabolism, and regulating cell processes. Without the ability to maintain NAD+ levels, the body’s immune system is severely compromised. For instance, you can not properly metabolize Vitamin C, Vitamin D, and zinc without NAD+. No matter how large of a megadose you take, it will not be metabolized; therefore, it will not be utilized in your immune response to any pathogen.

Not only will inadequate NAD+ levels impact your immune response, lack of NAD+ causes significant symptoms due to lack of cell regulation. A COVID NAD+ deficiency can cause a lack of serotonin regulation resulting in a lack of body temperature regulation. Dr. Ade Wentzel added, “NAD+ deficiency causes a lack of Tryptophan which is used for serotonin production and hence temperature…” Lack of cell and cytokine regulation also causes headaches, brain fog, anxiety, stress, loss of taste or smell, dizziness, fatigue, muscle aches, dermatitis, diarrhea, dementia, and death. Any activity that causes inflammation or a demand for NAD+ will result in more acute symptoms. Exercise and exertion of any kind exacerbates the condition.

The types of COVID-19 genome modifications are known as epigenetics. “Unlike genetic changes, epigenetic changes are reversible and do not change your DNA sequence, but they can change how your body reads a DNA sequence,” explains the CDC. At this time, we do not how many many genome modifications COVID makes nor how long the modifications will last.

Thousands of CISP patients have been treated successfully with a modified pellagra therapy; however, after a year of treatment, NAD+ production has not returned to normal for most patients.

In addition to genome modifications to NAD+, COVID also makes other changes. Brain fog, dizziness, tinnitus, ear aches, vertigo, and pressure in the ears are some of the symptoms associated with epigenetic changes in the upregulation of Indoleamine 2,3-dioxygenase (IDO). “IDO is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.’ (Wikipedia)

Dr. Ade Wentzel said, “The epigenetic upregulation of IDO will determine the amount of quinolinic acid. Quinolinic acid comes from the kynurenine pathway. If the viscosity of the whole middle ear is increased then the ability to equalize will be less… same as having a cold. So, the ear isn’t equalizing correctly on increasing pressure. The same as when you land in a plane. If the viscosity in the semicircular canals is increased, the otoliths may well be lagging causing the vertigo. The otoliths usually “Float” in the semicircular canal and trigger tiny sensory hairs that allow you to detect position.”

It is possible that changes in the weather that cause changes in atmospheric pressure (Lows and Highs) may result in the same problems.

There are many other Epifactors and Transcription Factors caused by COVID. “Using integrative analyses of gene co-expression networks and de-novo pathway enrichment, we characterize different gene modules and protein pathways enriched with Transcription Factors or Epifactors relevant for SARS-CoV-2 infection. We identified EP300, MOV10, RELA, and TRIM25 as top candidates, and more than 60 additional proteins involved in the epigenetic response during viral infection that has therapeutic potential. Our results show that targeting the epigenetic machinery could be a feasible alternative to treat COVID-19.” (Nature)

“We found that exposure to the SARS-CoV-2 spike protein alone was enough to change baseline gene expression in airway cells,” said Evans who is based in the laboratory of Sharilyn Almodovar, Ph.D., at the Texas Tech University Health Sciences Center.

“This suggests that symptoms seen in patients may initially result from the spike protein interacting with the cells directly.”

The researchers analyzed expression in genes with functions related to oxidative and osmotic stress, cell death, the inflammatory response, and DNA damage, among others. They found that expression of CCL2, IL1A, IL1B, and MMP9 showed up to two-fold changes in expression after recovery.

All of these genes play a role in inflammation. CCL2 levels are increased in neuroinflammatory disorders such as epilepsy and Alzheimer’s, as well as in some autoimmune diseases like psoriasis, whereas MMP9 is needed for wound healing and recovery from lung damage.

IL1A and IL1B are part of the interleukin family of cytokines and directly produce inflammation and promote fever, as well as playing a regulatory role in the greater immune response. —
— Clinical OMICs

Structural analyses have elucidated hot spots in viral binding domains, mutations, and specific proteins in the host such as the receptor angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease serine 2 (TMPRSS2) to be implicated in cell entry and viral infectivity. Furthermore, epigenetic changes that regulate chromatin structure have shown a major impact in genome stabilization and maintenance of cellular homoeostasis and they have been implicated in the pathophysiology of the virus infection. Epigenetic research has revealed that global DNA methylation along with ACE2 gene methylation and post-translational histone modifications may drive differences in host tissue-, biological age- and sex-biased patterns of viral infection. Moreover, modulation of the host cells epigenetic landscape following infection represents a molecular tool used by viruses to antagonize cellular signalling as well as sensing components that regulate the induction of the host innate immune and antiviral defence programmes in order to enhance viral replication and infection efficiency.
— Epigenetic mechanisms regulating COVID-19 infection (NIH)

“Viral proteins encoded by SARS-CoV-2 disrupt critical components of human cells’ molecular machinery and disable responses to infection. Researchers in the US describe how specific viral proteins bind to human RNAs involved in RNA splicing, protein translation, and protein trafficking, and in doing so suppress the host cell’s coordination of a key antiviral defense known as the type I interferon response.”
— SARS-CoV-2 Disables Key Components of Human Cells’ Defense System

“[COVID-19] interferes with protein trafficking to the cell membrane upon infection. Disruption of each of these essential cellular functions acts to suppress the interferon response to viral infection. Our results uncover a multipronged strategy utilized by SARS-CoV-2 to antagonize essential cellular processes to suppress host defenses.
— SARS-CoV-2 Disrupts Splicing, Translation, and Protein Trafficking to Suppress Host Defenses

COVID-19 genetic changes have been found to cause Reverse-transcribed SARS-CoV-2 RNA.

Prolonged detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA and recurrence of PCR-positive tests have been widely reported in patients after recovery from COVID-19, but some of these patients do not appear to shed infectious virus. We investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the DNA of human cells…
— Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be expressed in patient-derived tissues (PNAS)

How many different modifications to your genes does COVID-19 make? How long will the alterations last? We don’t know.

“Not all epigenetic changes are permanent. Some epigenetic changes can be added or removed in response to changes in behavior or environment.” Most of a person’s lifetime epigenetic changes have to do with aging. Infections and behaviors, like smoking, also can cause epigentic changes. Most of a smoker’s epigenetic changes revert back after a year of not smoking. Perhaps the COVID epigentic changes will go away over time. Unfortunately, COVID also does insertions. Insertions can not be reverted. The biggest unknown for COVID is the possibility — “if the insertion is in a tumor suppressor, for example, and disrupts that gene, then cancer can be a concern.”

Most experts are of the opinion that “the preexisting state may well determine the final outcome when there is genetic upregulation. COVID is choosing those that may well already have some subclinical symptoms of upregulated pathways.” In the case of cancer and tumor suppression, it appears COVID chooses people that have reduced P53 just like other coronavirus do (P53 is the tumor suppression gene.) Therefore, COVID is unlikely to cause insertions into the gene and be an additional cancer risk.

We do know there is upregulation of genes by COVID and these genes are related to abnormal T-cell, macrophage function, and abnormal humoral immunity. The epigenetic changes related to NAD+ have reverted in some cases after 13 months of treatment. The longer one has left it before getting help the harder and longer it takes for the epigenetics to revert. Currently, we are monitoring cases of epigenetic reversion as more people reach 12 months of treatment.

Post–COVID-19 Associated with Immune Cell Infiltration and Altered Gene Expression
COVID causes long-term immune dysfunction. “These findings indicate that T cell–mediated inflammation persists in the olfactory epithelium long after SARS-CoV-2 has been eliminated from the tissue, suggesting a mechanism for long-term post–COVID-19 smell loss.”

COVID-19 Chronic Conditions

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderAirborne, Aerosol, & Viral Load

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The primary mode of COIVD transmission is the inhalation of very small fine droplets and aerosolized virus.

Viral load is the amount of virus exposure. The greater the viral load the more severe the COVID symptoms.

The CDC reports:
SARS-CoV-2 is transmitted by exposure to infectious respiratory fluids

The principal mode by which people are infected with SARS-CoV-2 (the virus that causes COVID-19) is through exposure to respiratory fluids carrying infectious virus. Exposure occurs in three principal ways: (1) inhalation of very fine respiratory droplets and aerosol particles, (2) deposition of respiratory droplets and particles on exposed mucous membranes in the mouth, nose, or eye by direct splashes and sprays, and (3) touching mucous membranes with hands that have been soiled either directly by virus-containing respiratory fluids or indirectly by touching surfaces with virus on them.

People release respiratory fluids during exhalation (e.g., quiet breathing, speaking, singing, exercise, coughing, sneezing) in the form of droplets across a spectrum of sizes.1-9 These droplets carry virus and transmit infection.

The largest droplets settle out of the air rapidly, within seconds to minutes.
The smallest very fine droplets, and aerosol particles formed when these fine droplets rapidly dry, are small enough that they can remain suspended in the air for minutes to hours.

Infectious exposures to respiratory fluids carrying SARS-CoV-2 occur in three principal ways (not mutually exclusive):

Inhalation of air carrying very small fine droplets and aerosol particles that contain infectious virus. Risk of transmission is greatest within three to six feet of an infectious source where the concentration of these very fine droplets and particles is greatest.
Deposition of virus carried in exhaled droplets and particles onto exposed mucous membranes (i.e., “splashes and sprays”, such as being coughed on). Risk of transmission is likewise greatest close to an infectious source where the concentration of these exhaled droplets and particles is greatest.
Touching mucous membranes with hands soiled by exhaled respiratory fluids containing virus or from touching inanimate surfaces contaminated with virus.

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The risk of SARS-CoV-2 infection varies according to the amount of virus to which a person is exposed

Once infectious droplets and particles are exhaled, they move outward from the source. The risk for infection decreases with increasing distance from the source and increasing time after exhalation. Two principal processes determine the amount of virus to which a person is exposed in the air or by touching a surface contaminated by virus:

Decreasing concentration of virus in the air as larger and heavier respiratory droplets containing virus fall to the ground or other surfaces under the force of gravity and the very fine droplets and aerosol particles that remain in the airstream progressively mix with, and become diluted within, the growing volume and streams of air they encounter. This mixing is not necessarily uniform and can be influenced by thermal layering and initial jetting of exhalations.
Progressive loss of viral viability and infectiousness over time influenced by environmental factors such as temperature, humidity, and ultraviolet radiation (e.g., sunlight).

Transmission of SARS-CoV-2 from inhalation of virus in the air farther than six feet from an infectious source can occur

With increasing distance from the source, the role of inhalation likewise increases. Although infections through inhalation at distances greater than six feet from an infectious source are less likely than at closer distances, the phenomenon has been repeatedly documented under certain preventable circumstances.10-21 These transmission events have involved the presence of an infectious person exhaling virus indoors for an extended time (more than 15 minutes and in some cases hours) leading to virus concentrations in the air space sufficient to transmit infections to people more than 6 feet away, and in some cases to people who have passed through that space soon after the infectious person left. Per published reports, factors that increase the risk of SARS-CoV-2 infection under these circumstances include:

Enclosed spaces with inadequate ventilation or air handling within which the concentration of exhaled respiratory fluids, especially very fine droplets and aerosol particles, can build-up in the air space.
Increased exhalation of respiratory fluids if the infectious person is engaged in physical exertion or raises their voice (e.g., exercising, shouting, singing).
Prolonged exposure to these conditions, typically more than 15 minutes.

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderMore Than 900,000 People Have Died Of COVID-19 In U.S

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As of May 6, 2021, a new study estimates more than 900,000 have died from COVID in the USA (and more than 6.9 million globaly.)

The study, “COVID-19 has caused 6.9 million deaths globally, more than double what official reports show”, comes from scientists at the University of Washington’s Institute for Health Metrics and Evaluation. “As terrible as the COVID-19 pandemic appears, this analysis shows that the actual toll is significantly worse,” said Dr. Chris Murray, IHME’s director. “Understanding the true number of COVID-19 deaths not only helps us appreciate the magnitude of this global crisis, but also provides valuable information to policymakers developing response and recovery plans.”

The 20 countries with the highest number of total COVID-19 deaths, March 2020­–May 2021 

Country  Total COVID-19 deaths  Reported COVID-19 deaths 
United States of America 905,289 574,043
India 654,395 221,181
Mexico 617,127 217,694
Brazil 595,903 408,680
Russian Federation 593,610 109,334
United Kingdom 209,661 150,519
Italy 175,832 121,257
Iran 174,177 72,906
Egypt 170,041 13,529
South Africa 160,452 54,390
Poland 149,855 68,237
Peru 147,765 62,739
Ukraine 138,507 46,737
France 132,680 105,506
Spain 123,786 85,365
Germany 120,729 83,256
Indonesia 115,743 45,938
Japan 108,320 10,390
Romania 87,649 28,382
Kazakhstan 81,696 5,620

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bookmark_borderCOVID-19: A Survivor’s Story

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by Daniel Brouse

(Also see the update: 3 Years of Living With It)

I am a scientist and journalist publishing articles and papers since 1994. As part of a collective of scientists, we have been working on the greatest threat to humankind — humans. Much of my effort has been spent on Anthropogenic Climate Change. In addition, I have specialized in pollution, diseases, health and wellness.

In late December 2019 and early January 2020, I started studying a novel coronavirus discovered in Wuhan, China. My first paper on the subject was published in March 2020 entitled “COVID-19 and Air Pollution”.

In late January of 2020, I had been very ill with an upper respiratory illness. The same illness killed my father. At the time, COVID-19 had not been known in the USA. Since there was no test for COVID, the doctors could not diagnose the specific virus that caused my father’s death. It wasn’t until my recurring symptoms were diagnosed as “COVID Long Haulers” in May of 2020 that I knew I was suffering the aftermath of COVID-19.

The recurring symptoms were so concerning that I devoted all of my resources to studying COVID-long and searching for a cure. Every couple of weeks I went through a wave of symptoms. Though not as severe as the original illness, the symptoms still would render me useless. The symptoms did not come on all at the same time, rather they would cycle through over two weeks (not necessarily in the same order) and then repeat. Exercise and exertion would cause the symptoms to be more severe. The symptoms included:

* difficulty breathing (feeling like you’re not taking in enough oxygen)
* congestion / mild cough
* stomach issues / diarrhea
* loss of taste, smell, and appetite
* temperature regulation / night sweats
* nightmares / vivid dreams
* dizziness / the spins / foggy thinking
* headaches / body aches / soreness
* fatigue
* ear aches
* peripheral neuropathy (tingling of the hands and feet)

My concerns were several. Would the symptoms go away over time? As the months went on, the answer was no. Would the long term recurrence of systems cause a permanent disability? The answer is probably yes. My organs were sustaining progressive damage. Respiratory, circulatory, neurological, and renal damage, as well as, blood clots, thinning and leaky blood vessels in the brain tissue, and death have all been attributed to COVID and COVID-long.

In my pursuit of answers, I found another long hauler scientist, Dr. Ade Wentzel. Ade proved to me that my hypothesis of “COVID-19 Long Haulers: autoimmune response due to inactive particles of the virus” was incorrect. Rather, he demonstrated that sars-cov-2 causes COVID-19 Induced Secondary Pellagra (CISP).

The main culprit is believed to be COVID’s genetic change to our production and utilization of NAD+ (nicotinamide adenine dinucleotide). NAD+ is involved in cell creation, maintenance, metabolism, and regulating cell processes. COVID can chronically increase the breakdown of NAD+ and simultaneously decrease the production of NAD+.

Ade added, “The biggest function of NAD+ is as a cofactor for energy(atp) production via the citric acid cycle. NAD+ is essential for carbohydrate metabolism. The brain being highly dependent on carbs.”

NAD+ and the Citric Acid Cycle
NAD+ and the Citric Acid Cycle

Ade introduced me to one of the co-authors of his research, Robert Miller. In October of 2020, Ade and Robert started me on “the stack”. The vitamin stack helps correct the NAD+ malady by treating COVID-19 Induced Secondary Pellagra. Finding the correct form and dosage of Niacin was the most challenging part.

Within days of starting the stack, my COVID-long symptoms dissipated. Since that time, I have remained relatively symptom free EXCEPT when I tried reducing the Niacin dosage. On three separate occasions, I experimented with reducing the dosage of Niacin. All three times my symptoms returned; therefore, I would call the stack a treatment not a cure.

Since that time, I have successfully helped thousands of other COVID-long victims with the stack.

At the end of April, I received my first dose of the Moderna vaccine. Loss of taste and muscle soreness symptoms returned for 24 hours and then disappeared. My overall wellness appears to have improved. Now, I’m experimenting with reducing my Niacin dosage again to see if the vaccine helped my body recover its ability to produce and retain NAD+.

After several days of reduced Niacin (nicotinic acid dosage was reduced from 300-500mg/day down to 0-30mg day), symptoms returned: neuropathy, fatigue, brain fog, muscle soreness, difficulty breathing, GI track / stomach issues, ear aches, and allergy-like symptoms. The most notable symptom to return — headaches. Prior to COVID, I did not experience headaches. Within days of decreasing the dosage, a chronic headache returned. I increased the Niacin dosage back to 500mg/day and supplemented the stack with resveratrol. Symptoms immediately dissipated.

After the second shot, side-effects were slightly worse. The metallic taste returned within a couple hours. For the 12-24 hours post-vaccination, there was dizziness, nausea, and fatigue. Then, all the side-effects disappeared. Three months after being fully vaccinated all of my presenting symptoms dissipated. Other “silent” post COVID conditions have persisted since the initial infection.

See the update: 3 Years of Living With It

CISP and The Stack

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus