Health, Fitness,Dite plan, health tips,athletic club,crunch fitness,fitness studio,lose weight,fitness world,mens health,aerobic,personal trainer,lifetime fitness,nutrition,workout,fitness first,weight loss,how to lose weight,exercise,24 hour fitness,
As the world emerges from lockdown due to the pandemic, many peculiarities exist that have led a growing number of people to question whether the pandemic is real or orchestrated in some way, and if the latter is true, toward what end?
Many are not aware that before the pandemic even started, Johns Hopkins Center for Health Security, the World Economic Forum and the Bill & Melinda Gates Foundation sponsored a novel coronavirus pandemic preparedness exercise.
The event, which took place October 18, 2019, in New York City, was called "Event 201," and it included a detailed simulation of a coronavirus outbreak with a predicted global death toll of 65 million people within a span of 18 months.1
Meanwhile, we are repeatedly told that COVID-19 originated from a wild animal at the Huanan Seafood Market in Wuhan, China, and that it is a natural mutation of a bat virus. But the hard evidence contradicts this theory, while evidence grows that it may actually be a man-made virus that was leaked, either accidentally or intentionally.
Then there are the questions about the death toll. Without an accurate test to isolate the virus, and seeing how “suspected” cases are lumped into mortality statistics, accurate mortality rates are elusive. To date, however, with most of those affected appearing to be asymptomatic,2 COVID-19 simply doesn’t warrant the draconian elimination of personal freedom and liberty we’re currently seeing.
Nor is it serious enough to warrant the kinds of long-term surveillance strategies suggested by Bill Gates and The Rockefeller Foundation. Yet here we are.
In a press release quietly released March 19, 2020, the United Nations New World Order (UNNWO) launched a campaign to celebrate an “International Day of Happiness” on March 20, 2020.3 If you haven’t heard of UNNWO, its website starts out with, “Let’s take our planet back,” then reads:4
“Lets stand united. Lets stand together. The New World Order Project is an independent international campaign to advance the principles, values, and articles of the UN Charter, and UN resolutions 65 309, and 66 281, in support of the UN’s Global Goals for Sustainable Development by 2030, and the happiness, well-being, and freedom of all life on Earth by 2050.”
Its initiatives include “happytalism,” which “places happiness, well-being and freedom at the center of human development models, systems and all life.” It also supports the mobilization of more than $30 trillion toward achieving the 17 UN Global Goals by 2030, which include things like no poverty, zero hunger, gender equality and clean water and sanitation.
It sounds like utopia, but some believe the push for a one-world government isn’t about pushing forward world peace and happiness but, rather, about taking rights away from the public and putting the power into the hands of a select few.5 Censorship of media and social media is already filtering information and telling people what they should and shouldn’t fear, and increased surveillance is being pushed courtesy of coronavirus.
The World Health Organization also has an Immunization Agenda 2030, in which they’re aiming to vaccinate everyone across the globe: “IA 2030 envisions a world where everyone, everywhere, at every age, fully benefits from vaccines to improve health and well-being.”6 The Bill & Melinda Gates Foundation is the biggest funder of WHO, and Bill Gates intends to vaccinate the global population against COVID-19, and then track and monitor each one through digital surveillance.
There’s no reason in the world to believe this gigantic global disease surveillance system would be dismantled once the pandemic is declared over. Naturally, it will simply transition into other surveillance functions.
The Rockefeller Foundation has a plan to test, track and trace all Americans — ostensibly to prevent COVID-19 from overwhelming us as we’re again “allowed” to venture outside our front doors in limited capacity around the nation.
The Rockefeller Foundation’s April 21, 2020, white paper, “National COVID-19 Testing Action Plan — Strategic Steps to Reopen Our Workplaces and Our Communities,”7 lays out a strategic framework that is clearly intended to become part of a permanent surveillance and social control structure that severely limits personal liberty and freedom of choice.
The Rockefeller plan calls for COVID-19 testing and tracing of 1 million Americans per week to start, incrementally ramping it up to 3 million and then 30 million per week (the “1-3-30 plan”) over the next six months until the entire population has been covered.
Contact-tracing apps are a significant part of this scheme, and some contact-tracing apps require you to keep your cellphone on your person throughout the day, giving thousands of third parties access to personal data. Contract tracing also entails tracing and monitoring contacts of infected people, notifying them of their exposure and supporting the quarantine of contacts.8
In May 2020, Johns Hopkins launched an online course to train “an army” of contact tracers, for which hundreds of people joined within hours of its release. Those who take the course will be trained to interview people diagnosed with COVID-19, identify their close contacts who might have been exposed and then give them guidance on how to self-quarantine for two weeks.9
Anyone can take the free six-hour course, but passing it and receiving certification is required for anyone who will be hired by the state of New York to “fight the pandemic.”10 If you’re wondering what it actually entails, the video above follows one woman’s experience getting her contact tracer certificate.
What they’re being taught, for starters, is that if you’re sick, you must stay in isolation for a minimum of 10 days after onset and with no fever for three days. This includes being isolated from family members and household pets, which you cannot snuggle or pet.
You may have to go into a hotel room if you don’t have any way to isolate your bathroom, for instance, from the rest of your family. And, according to the video, the contact tracer “will check that out” and you’ll have to provide video evidence showing that you have the space to be isolated.
If you’re healthy but have been in contact with someone who had the disease, you have to be quarantined for 14 days, meaning you can’t leave your house. “Unfortunately,” the woman states on the video, “you could be totally healthy, get out of quarantine and guess what, someone else in the vicinity in a restaurant has it and you could end up quarantined again.”
If you test positive, the contact tracer will also work with you to figure out who you came into contact with. They’ll go through your phone and social media with you to help jog your memory, and will ask for any movies you’ve seen, flights you’ve been on, people you work with, family, restaurants you’ve visited and more. Everyone whose path you crossed would also be quarantined.
While it’s been said that quarantine will be voluntary, some related documents state that if you do not comply, police may enforce a detention order to assure compliance. It’s also stated in some states that you can be fined up to $2,000 a day or incarcerated for not staying in quarantine.
The course informs contact tracers that what they’re doing is for the greater good and basically that while everyone has a right to their privacy, when it comes to “the greater good,” your privacy is null and void. COVID-19 test results will be automatically sent into an electronic database, and tracers will get your information if you test positive, whether you want them to or not.
The resulting isolation and quarantines can be mandated and enforced, as can other health enforcements, like vaccines and medications.
In 2010, The Rockefeller Foundation released a report, “Scenarios for the Future of Technology and International Development,” which uses scenario planning to explore ways that technology and growth/development and government might play out over the coming decades. One of the scenarios they detailed was a pandemic with some eerie similarities to COVID-19:11
“In 2012, the pandemic that the world had been anticipating for years finally hit. Unlike 2009’s H1N1, this new influenza strain — originating from wild geese — was extremely virulent and deadly.
Even the most pandemic-prepared nations were quickly overwhelmed when the virus streaked around the world, infecting nearly 20 percent of the global population and killing 8 million in just seven months, the majority of them healthy young adults.
The pandemic also had a deadly effect on economies: international mobility of both people and goods screeched to a halt, debilitating industries like tourism and breaking global supply chains. Even locally, normally bustling shops and office buildings sat empty for months, devoid of both employees and customers.”
The scenario suggests that China fared far better than the U.S., due to its government’s “quick imposition and enforcement of mandatory quarantine for all citizens, as well as its instant and near-hermetic sealing off of all borders, saved millions of lives, stopping the spread of the virus far earlier than in other countries and enabling a swifter post- pandemic recovery.”
As the pandemic continues, “national leaders around the world flexed their authority and imposed airtight rules and restrictions, from the mandatory wearing of face masks to body-temperature checks at the entries to communal spaces like train stations and supermarkets.” The increased authoritarian control and oversight of citizens continued even after the pandemic ended, and was welcomed at first in exchange for “greater safety and stability.”
Eventually, however, things began to unravel. “By 2025, people seemed to be growing weary of so much top-down control and letting leaders and authorities make choices for them … The feeling lingered that sooner or later, something would inevitably upset the neat order that the world’s governments had worked so hard to establish,” the report reads.12
There is also the suggestion that in another outcome, governments could weaken, leading to a world in which “criminals thrive and dangerous innovations emerge.”
In another outcome, painted as the more desirable “clever together,” philanthropic organizations collaborate with governments, businesses and NGOs to improve standards of living around the globe, working with government to make it stronger and using technology toward that end but, in reality, what we’re seeing is a movement toward foundations moving toward taking rights away from people.
At this point, signs that an all-encompassing global totalitarian plan is being quietly put together, piece by piece, are all around us. The Rockefeller Foundation's white paper calls for the use of a digital "patient identification number" to track all Americans after testing them for COVID-19.13
Meanwhile, Gavi, the Vaccine Alliance, set up with funds from the Bill & Melinda Gates Foundation, has partnered with the ID2020 Alliance to launch a digital identity program called ID2020 in Bangladesh.14 Your health information, in the form of COVID-19 test results, are set to be sent to an electronic database so that contact tracers can enforce isolation and quarantines, even if you’re healthy.
There are even plans for a global currency. Google, Gates and The Rockefeller Foundation announced the formation of Mojaloop, which is open-source software designed to be used for financial transactions. The technology is modeled after M-Pesa from Nigeria, which has been successful since 2007. Mojaloop is intended to be managed by governments or financial authorities.15
The Rockefeller Foundation and Gates are not presenting short-term, temporary measures. They’re both aiming to implement a totalitarian control system. It’s not so far-fetched to imagine a future in which your vaccine certificate or “unique patient ID number” replaces personal identifications such as your driver’s license, state ID card, Social Security card and passport, and is tied not only to your medical records in total, but also your finances.
The U.S. Centers for Disease Control and Prevention’s provisional death counts for COVID-19 show a striking change. While starting at zero in February 2020 and spiking up to more than 5,000 deaths per week for the oldest age range (85 and over) and 111 among 25- to 34-year-olds in late April, they’ve plummeted.
There were 199 COVID-19 deaths for the week ending May 30, 2020, among those 85 and over, while only one death was reported among 25- to 34-year-olds — an extremely rapid decline from April to May.1 What happened to make the deaths come to a standstill, according to some experts, might be the same seasonal ebb and flow that happens with many respiratory infections: Summer may have killed it.
While it’s possible to get respiratory infections like influenza any time of year, influenza is more common during the fall and winter, hence the “flu season” during those months. Respiratory syncytial virus (RSV), a leading cause of severe respiratory illness in young children and those aged 65 and over, is also more common in the fall and winter.
At least four common coronaviruses are also highly seasonal with transmission similar to influenza.2 Although these aren’t related to SARS-CoV-2, the virus that causes COVID-19, it is genetically related to the coronavirus responsible for the severe acute respiratory syndrome (SARS) outbreak of 2003.
This is notable because, as noted by professor Paul Hunter from the University of East Anglia in England, “Sars largely spread in hospitals but still died out in the summer in the Northern Hemisphere.”3 There are a number of reasons why SARS was quickly contained in about eight months, but the summer, with its higher temperature and humidity level, is among them.
Winter’s dry, cold air is favorable to the spread of flu transmission, and influenza spread is known to be affected by both temperature and humidity.4 During the winter, people also spend more time indoors, in enclosed spaces with less ventilation and less personal space compared to being outdoors in the summer.5
School is usually in session during the fall and winter, with students at home over the summer. School terms have been associated with higher transmission of respiratory viruses, while holidays lead to a 20% to 29% reduction in the rate at which influenza is transmitted in children.6 So, just the fact that children are in school in the winter may raise transmission rates.
What’s more, as noted by Marc Lipsitch, professor of epidemiology and director of the Center for Communicable Disease Dynamics at the Harvard T.H. Chan School of Public Health:7
“It is possible that the condition of the average person’s immune system is systematically worse in winter than summer. One hypothesis has focused on melatonin which has some immune effects and is modulated by the photoperiod, which varies seasonally. Another with more evidence is that vitamin D levels, which depend in part on ultraviolet light exposure (higher in summer) modulate our immune system in a positive way.”
A number of studies have suggested COVID-19 may, in fact, taper off during the summer. One preprint study tracked the seasonality of influenza viruses and endemic human coronaviruses over an eight-year period. The activity of human coronaviruses peaked the first week of January, with transmission facilitated by low indoor relative humidity (RH) of 20% to 30%.8
The researchers cited previous studies that found an increase in relative humidity to 50% reduced the transmission of both influenza and animal coronaviruses. What’s more, the study found a decrease in disease incidence by 50% in early March, 75% in early April and greater than 99% at the end of April. According to the study:9
“As a lipid-bound, enveloped virus with similar size characteristics to endemic human coronaviruses, SARS-CoV-2 should be subject to the same dynamics of reduced viability and transmission with increased humidity. In addition to the major role of social distancing, the transition from lower to higher indoor RH with increasing outdoor temperatures could have an additive effect on the decrease in SARS-CoV-2 cases in May.
Over the 8-year period of this study, human coronavirus activity was either zero or >99% reduction in the months of June through September, and the implication would be that SARS-Cov-2 may follow a similar pattern.”
A study conducted in Sydney, Australia, found a similar connection between humidity and COVID-19. A 1% decrease in humidity was predicted to increase the number of cases by 6.11%,10 with researchers stating, “During periods of low relative humidity, the public health system should anticipate an increased number of COVID‐19 cases.”11
Professor Michael Ward, an epidemiologist in the Sydney School of Veterinary Science at the University of Sydney, said in a news release that humidity appeared to be a major factor:12
"When it comes to climate, we found that lower humidity is the main driver here, rather than colder temperatures. It means we may see an increased risk in winter here, when we have a drop in humidity. But in the northern hemisphere, in areas with lower humidity or during periods when humidity drops, there might be a risk even during the summer months.
… When the humidity is lower, the air is drier and it makes the aerosols smaller. When you sneeze and cough those smaller infectious aerosols can stay suspended in the air for longer. That increases the exposure for other people. When the air is humid and the aerosols are larger and heavier, they fall and hit surfaces quicker."
Aside from affecting transmission rates, humidity may also affect the survival of viruses. The addition of a portable humidifier with an output of 0.16 kilograms of water per hour in the bedroom increased absolute humidity 11% and relative humidity 19% during sleeping hours compared to having no humidifier present, according to one study. Along with the increases in humidity came a decrease in the survival of influenza virus, by 17.5% to 31.6%.13
Humidity even influences innate immune defenses against viral infections. In an animal study, dry air compromised the mice’s resistance to infection, and those housed at lower humidity levels had impaired mucociliary clearance, innate antiviral defense and tissue repair function, the study found.14
The other reason why summer may slash COVID-19 deaths is because summer equals greater exposure to sunlight, which boosts vitamin D levels. There is strong scientific evidence vitamin D plays a central role in your immune response and your ability to fight infections. It’s been shown in an analysis of 212 people with lab-confirmed COVID-19 that disease severity is associated with vitamin D levels, with lower levels linked to more severe disease.15
A review published in the journal Nutrients also concluded that not only could vitamin D be useful to reduce the risk of infection with COVID-19, but also could be helpful for treatment:16
“Evidence supporting the role of vitamin D in reducing risk of COVID-19 includes that the outbreak occurred in winter, a time when 25-hydroxyvitamin D (25(OH)D) [vitamin D] concentrations are lowest; that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome; and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration.”
If COVID-19 is seasonal, a resurgence is likely come fall, which is why the time for optimizing your vitamin D level is now. To improve your immune function and lower your risk of viral infections, you’ll want to raise your vitamin D to a level between 60 nanograms per milliliter (ng/mL) and 80 ng/mL by fall. In Europe, the measurements you’re looking for are 150 nanomoles per liter (nmol/L) and 200 nmol/L.
Harvard professor Lipsitch is among those who said COVID-19 would “probably not” go away on its own in warmer weather. “The short answer is that while we may expect modest declines in the contagiousness of SARS-CoV-2 in warmer, wetter weather and perhaps with the closing of schools in temperate regions of the Northern Hemisphere, it is not reasonable to expect these declines alone to slow transmission enough to make a big dent,” he said.17
CDC’s provisional death counts appear to suggest otherwise, but some have cautioned that COVID-19 is too new to be seasonal. In other words, because fewer people have established immunity, a new virus has an advantage in that it can thrive even in less-than-optimal conditions for a virus, i.e., the summer.
“Old viruses,” Lipsitch said, “which have been in the population for longer, operate on a thinner margin — most individuals are immune, and they have to make do with transmitting among the few who aren’t.”18
Likewise, a study in Science used a computer model to suggest that while COVID-19 may fall into seasonal patterns eventually, this may not occur until more people develop immunity, noting that “susceptible supply” is limiting the role of climate in the early COVID-19 pandemic.19
The drastic decline in COVID-19 deaths that occurred from April to May do suggest a seasonal component, but what’s driving the drop is not completely understood. It’s likely a combination of humidity, heat, human behaviors, vitamin D levels and, likely, other aspects of sunlight exposure that are culminating in this decline.
With summer upon us in the U.S., you can use it to your advantage to spend time outdoors, optimize your vitamin D levels and get sensible sun exposure, all of which can help you support health and reduce your susceptibility to viral infections.
Chinese authorities have finally admitted SARS-CoV-2 did not originate in a Wuhan wet market,1 but that’s about as far as we’ve gotten to getting an official answer to the question about where the virus came from. Many valid questions are being raised, and have continued to be raised about the possibility that it is in fact manmade.
Evidence indicating it is an engineered virus include the Antiviral Research paper2 “The Spike Glycoprotein of the New Coronavirus 2019-nCoV Contains a Furin-Like Cleavage Site Absent in CoV of the Same Clade,” published in April 2020, and “Furin, a Potential Therapeutic Target for COVID-19,”3,4 posted in February 2020.
According to these papers, SARS-CoV-2 is the only coronavirus with a furin cleavage site. Not even distant relatives of SARS-CoV-2 have it, and the coronaviruses that do have it share only 40% of SARS-CoV-2’s genome.5,6 Attempts have, however, been made to introduce a furin cleavage site onto the spike of a coronavirus, and successfully so.7
While neither of these papers makes any claims about how this gain-of-function might have come about, others have pointed out that this novel function couldn’t possibly have arisen naturally. I summarized Chris Martenson’s8 and Yuri Deigin’s9 reviews of these findings in “The Smoking Gun Proving SARS-CoV-2 Is an Engineered Virus.”
Others have pointed out that viruses can easily be manipulated and altered using low-tech methods that do not leave telltale signs of genetic insertion or interference. One such method is known as “passaging.” As reported by Independent Science News:10
“Passaging is the placing of a live virus into an animal or cell culture to which it is not adapted and then, before the virus dies out, transferring it to another animal or cell of the same type. Passaging is often done iteratively.
The theory is that the virus will rapidly evolve (since viruses have high mutation rates) and become adapted to the new animal or cell type. Passaging a virus, by allowing it to become adapted to its new situation, creates a new pathogen.
The most famous such experiment11 was conducted in the lab of Dutch researcher Ron Fouchier. Fouchier took an avian influenza virus (H5N1) that did not infect ferrets (or other mammals) and serially passaged it in ferrets. The intention of the experiment was specifically to evolve a PPP [potential pandemic pathogen].
After ten passages the researchers found that the virus had indeed evolved, to not only infect ferrets but to transmit to others in neighboring cages. They had created an airborne ferret virus, a Potential Pandemic Pathogen, and a storm in the international scientific community.”
In a June 3, 2020, Telegraph interview,12,13 former MI6 chief (yes, folks the same MI6 in James Bond movies) Sir Richard Dearlove discussed a scientific report that suggests key elements of the virus were strategically inserted to make it infectious to humans.
According to The Telegraph,14,15 Dearlove “believes the coronavirus pandemic ‘started as an accident’ when the virus escaped from a laboratory in China.” If proven true, it could have significant economic ramifications for China. It may even be called on to pay reparations for the economic devastation caused by the pandemic around the world.
That said, it’s important to recognize that the issue of SARS-CoV-2’s origin is not a racial, cultural or political one. The real issue here is whether or not dangerous gain-of-function research is wise and whether it should be allowed to continue — anywhere.
For years, such research has been conducted all over the world, and it’s no longer a secret the U.S. funded the research in China that is now suspected of being the source of the COVID-19 pandemic.
Of course, the U.S. doesn’t want to implicate its own agencies in the creation of this virus, which is why government officials focus on the source of the leak — China — rather than the fact that it’s engineered. Clearly, if it’s engineered, everyone associated with its creation, including those funding it, would be responsible.
So, please, when discussing the origin of SARS-CoV-2, let us be crystal clear on what the problem is, namely dangerous bioweapons/biodefense research, not the Chinese population or its government per se. We need to point the finger at ALL researchers — regardless of the location of the laboratory — involved in these kinds of experiments.
If SARS-CoV-2 is an engineered manmade virus, it is proof positive that gain-of-function research poses tremendous risks to humanity and that those risks far exceed any potential gain. Virtually all other threats to humanity — environmental toxins, pesticides, GMOs, pollution — pale in comparison to the danger posed by biodefense/bioweapons research.
“Gain-of-function” refers to experiments in which a pathogen is altered to give it new or added functionality, such as the ability to infect humans, when before it could not, or increased infectiousness or lethality, for example.
A decade ago, Dr. Anthony Fauci defended and promoted gain-of-function research on bird flu viruses, saying such research was worth the risk because it allows scientists to prepare for pandemics.16
In reality, this kind of research does not appear to have improved governments’ pandemic responses at all. As noted in the 2016 paper,17 “Gain-of-Function Research: Ethical Analysis,” even if gain-of-function research were to lead to improved and effective control measures, laboratory accidents or “malevolent action” in which souped-up pathogens are released can result in casualties numbering in the millions.
We’ve now also seen what it can do to economies around the world. Biosafety level 3 and 4 facilities around the world have suffered repeated safety lapses,18,19 so it was really just a matter of time before something got out that had the ability to rapidly spread.
As noted in a 2013 paper,20 “controllability of escape events is not guaranteed and, given the rapid increase of biosafety laboratories worldwide, this poses a serious threat to human health.”
Indeed, the risk of a laboratory release is rather immense. As reported in the paper “The Consequences of a Lab Escape of a Potential Pandemic Pathogen,” published in the journal Frontiers in Public Health in 2014:21
“The first Department of Homeland Security risk assessment for the planned National Bio- and Agro-Defense Facility in Manhattan, Kansas estimated a significantly higher escape risk, over 70% likelihood for the 50-year life of the facility, which works out to be a basic probability of escape, p1 = 2.4% per year.
The National Research Council overseeing the risk assessment remarked ‘The … estimates indicate that the probability of an infection resulting from a laboratory release of FMDv from the NBAF in Manhattan, Kansas approaches 70% over 50 years … with an economic impact of $9-50 billion.
The committee finds that the risks and costs could well be significantly higher than that…’ While the DHS subsequently lowered the escape risk to 0.11% for the 50-year lifetime, the NRC committee was highly critical of the new calculations:
‘The committee finds that the extremely low probabilities of release are based on overly optimistic and unsupported estimates of human error rates, underestimates of infectious material available for release, and inappropriate treatment of dependencies, uncertainties, and sensitivities in calculating release probabilities.’ We have more trust in the NRC committee conclusions, as they have no skin in the game.”
Yet another paper, published in May 2016 in The Journal of Infectious Diseases noted:22
“The recent safety lapses at the Centers for Disease Control and Prevention and the NIH that could have resulted in exposure to anthrax and smallpox, respectively, have diminished public confidence in the ability of even high-containment laboratories to mitigate the risk of accidental release of pathogens of potential harm ...
Public tolerance of that risk may be the ultimate determinant of what types of research are allowed to proceed … As recent lapses at high profile laboratories have illustrated, there remains the potential that bacterial and viral strains can escape even the most secure environments.”
In his interview, Dearlove highlights a recent paper23 in the journal Quarterly Review of Biophysics Discovery by Norwegian and British researchers Sorensen, Susrud and Dalgleish.
Like the two papers previously mentioned, this one also claims to have identified inserted sections in the spike surface that allows it to bind to and enter human cells. According to the authors, “The SARS-CoV-2 spike is significantly different from any other SARS that we have studied.”
Importantly, Sorensen’s paper warns that current efforts to develop a COVID-19 vaccine are likely to fail simply because the etiology of the virus has been misunderstood. According to this paper:24
“These data reveal the biological structure of SARS-CoV-2 Spike and confirm that accumulated charge from inserts and salt bridges are in surface positions capable of binding with cell membrane components other than the ACE2 receptor.
We have also looked at the naked coronavirus spike protein as a concept for the basis of a vaccine, which we have rejected because of high risk of contamination with human-like epitopes.
Analysis of the Spike protein of SARS-CoV-2 shows 78.4% similarity with human-like (HL) epitopes. For the avoidance of confusion, a standard protein blast searches for functionalities and homologies to other proteins.
However, antibodies can only recognize 5-6 amino acids and therefore a 6 amino acid rolling window search for antibody epitopes was performed.
A search so tailored to match against all human known proteins will give a 78.4% human similarity to the SARS-CoV-2 Spike protein, i.e if all epitopes on the 1255 amino acid long SARS-CoV-2 Spike protein can be used by antibodies then there will be 983 antibody binding sites which also could bind to epitopes on human proteins.
This is what we did and found … [I]n the present context, any vaccine design based on the whole Spike protein of SARS-CoV-2 may not be immunogenic due its high human similarity compared to a vaccine with specifically selected NHL epitopes, such as Biovacc-19 does — and is.
Covid-19 candidate vaccines designed without appreciating these problems may run similar risks to those experienced with HIV vaccines that failed to show protection.
The possibility of inducing autoimmune responses or antibody-dependent enhancements, needs to be carefully guarded against because there is published evidence that an HIV candidate vaccine has actually enhanced infectivity:
‘Vaccinations were halted; participants were unblinded. In post hoc analyses, more HIV infections occurred in vaccinees vs placebo recipients in men who had Ad5-neutralizing antibodies and/or were uncircumcised. Follow-up was extended to assess relative risk of HIV acquisition in vaccinees vs placebo recipients over time.’
Such antibody-dependent enhancement (ADE) has been observed for coronaviruses in animal models, allowing them to enter cells expressing Fc𝛾R. ADE is not fully understood: however, it is suggested that antibody-dependent enhancements may come as a result of amino acid variability and antigenic drift.”
They also point out that choosing an adjuvant after the primary vaccine design work has been completed, which is how vaccine development is typically done, may be yet another serious mistake that could make a COVID-19 vaccine really dangerous.
For all of these reasons, the researchers are now in the process of developing their own version of a vaccine, which will be produced by the Norwegian drug company Immunor AS. Dearlove believes this paper may finally shift the debate on SARS-CoV-2’s origin.
According to The Telegraph,25,26 in an earlier version the paper, which has reportedly been rewritten several times, Sorensen et al. claimed they had proven “beyond reasonable doubt that the COVID-19 virus is engineered.” That statement is no longer included in the paper.
Perplexingly, the Journal of Virology and Nature both rejected the paper, stating it was “unsuitable for publication.” Meanwhile, Nature has accepted Chinese studies rife with conflicts of interest that denounce the claim that SARS-CoV-2 may be a lab-created virus.
Sorensen’s paper was eventually accepted by Quarterly Review of Biophysics Discovery, a journal chaired by Stanford University and University of Dundee scientists.
Sorensen et al have also written an as-yet unpublished paper in which they reportedly claim SARS-CoV-2 has unique fingerprints that could not have evolved through natural means and are “indicative of purposive manipulation.” According to The Telegraph:27,28
“Entitled ‘A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike,’ the new study, seen by The Telegraph, suggests the virus is ‘remarkably well-adapted virus for human co-existence’ and is likely to be the result of a Wuhan lab experiment to produce ‘chimeric viruses of high potency.’
The paper concludes: ‘Henceforth, those who would maintain that the Covid-19 pandemic arose from zoonotic transfer need to explain precisely why this more parsimonious account is wrong before asserting that their evidence is persuasive, most especially when, as we also show, there are puzzling errors in their use of evidence.’"
A vaccine is now the most coveted “cure” for COVID-19, but mounting evidence suggests a mass vaccination campaign might ultimately end the vaccine dogma altogether by causing mass casualties.
As reported in “Newborns To Be Separated From Parents for COVID-19 Testing,” Bill Gates recently stated on his blog29,30 that “the COVID-19 vaccine might become part of the routine newborn immunization schedule.” This, despite the fact that COVID-19 presents virtually no risk to children and only three children have died from alleged COVID-19 illness in the U.S. — and even those deaths, as of June 8, 2020, had not yet had COVID-19 confirmed as the likely cause of death.31
While many have expressed concern about testing the fast-tracked COVID-19 vaccine on children, the University of Oxford in partnership with the drug company AstraZeneca have announced their plan to do just that.32 The vaccine, known only as AZD1222, is a recombinant adenovirus vaccine.
Phase 2 of the trial will include “a small number” of children between the ages of 5 and 12.33 Disturbingly, a meningococcal vaccine — not an inert placebo — will serve as the control, and participants are only asked to log symptoms occurring in the week after vaccination. According to Fierce Biotech:34
“… it will take longer to gauge whether the shot can prevent people from becoming infected with the coronavirus. The researchers are trying to accelerate that process by enrolling healthcare workers and other people who are more likely to be exposed to the virus.
Depending on the extent to which SARS-CoV-2 is present in the U.K., it is expected to take two to six months for enough infections to happen to show whether the vaccine is working.
Neither the university nor AstraZeneca are hanging around to see if that is the case before preparing for widespread use of the vaccine. The phase 2/3 trial is getting underway despite the university being yet to share phase 1 data, and AstraZeneca is already racing to equip itself to ship 1 billion doses.”
As discussed in “Fast-Tracked COVID-19 Vaccine — What Could Go Wrong?” and stressed in Sorensen’s Quarterly Review of Biophysics Discovery paper35 discussed earlier, if the vaccine ends up having the same problem as previous coronavirus vaccines, they could make exposure to the wild virus all the more dangerous, actually raising your risk of very serious infection and death by inducing paradoxical immune enhancement.
Indeed, as reported in “Expect Coronavirus Vaccine Failures and Reactions,” we’re already seeing early indications of vaccine failures and severe reactions in adults,36 although none have reported outright lethal effects in the short term.
One vaccine, referred to only as ChAdOx1 nCoV-19, developed at the University of Oxford Jenner Institute, uses a "replication-deficient chimpanzee adenovirus to deliver a SARS-CoV-2 protein to induce a protective immune response."37
Six rhesus macaque monkeys received the vaccine and were then infected with SARS-CoV-2 28 days later. The monkeys that received the vaccine had the same amount of coronavirus in their noses as three unvaccinated monkeys used as controls.38,39,40 In other words, all the vaccinated animals were infected to the same degree as the unvaccinated ones.
Equally concerning, the titer of neutralizing antibodies, which stop viruses from entering cells, was extremely low. While neutralizing antibodies from effective vaccines can be diluted by 1,000-fold and still be active, the neutralizing antibodies in this study could only be diluted up to 40-fold before becoming inactive.
This raises serious questions about its long-term effectiveness. If a vaccine stops working in months or weeks, then what’s the point? Despite all of these questions, the health law section of the New York State Bar Association (NYSBA) is calling for mandatory COVID-19 vaccination for all New Yorkers. As reported by NYSBA May 28, 2020:41
“The Health Law Section said a rapid mass vaccination plan should be launched in New York as soon as a safe and viable vaccine becomes available, citing Jacobson v. Massachusetts, a 1905 U.S. Supreme Court case that upheld the authority of states to enforce compulsory vaccination laws.
The plan should also prioritize vaccines for essential health care workers and vulnerable New Yorkers who are at highest risk of infection, the report states.”
I’ve said it before and I’ll say it again: If you have any concerns about mandatory COVID-19 vaccination at all, be sure to sign up for the National Vaccine Information Center’s Advocacy Portal — a free online communications tool that monitors vaccine-related state legislation and alerts residents when proposed bills are moving in their state.
They also provide fact-based talking points you can share when contacting your legislators. As a nation, we must stand up against government overreach and defend our right to medical freedom of choice.
By now, I’m sure you’ve all noticed that our rights are being ripped away at increasing speed, so even if you think a particular vaccine might be a candidate for forced vaccination, remember there is literally no limit to the number and types of vaccines the government can impose on us if we lose the right to choose.
There also will be nothing to stop them from seeking to expand mandates into other areas of medicine. How would you like to be forced to take a specific drug or have a particular medical procedure done if you’re diagnosed with a condition?
>>>>> Click Here <<<<<
It is important to remember that, although the U.S. Supreme Court decision in 1905, Jacobson v. Massachusetts, affirmed the constitutional authority of elected representatives in state legislatures to pass public health laws requiring vaccination, state legislators also have the constitutional authority to choose NOT to mandate vaccines and/or to include flexible medical, religious and conscientious belief exemptions in state public health laws.
Obstructive sleep apnea (OSA) is a disorder characterized by repeated episodes of partial or total upper airway obstruction that result in arousals from sleep, and changes in oxygen levels during sleep. OSA is one of the most common conditions I see as a sleep medicine specialist. This is not surprising, considering that OSA is estimated to affect about 20% of the general population, and is even more prevalent in patients who are obese, or who have heart or metabolic conditions like diabetes.
When untreated, OSA can negatively impact cardiac and metabolic health, quality of life, and result in excessive daytime sleepiness, insomnia, problems with thinking, and depression or anxiety. OSA impacts people of all ages, backgrounds, shapes, and sizes, and while both patients and doctors have become increasingly aware about OSA and its effects over recent years, about 80% of patients with OSA still go undiagnosed.
The severity of OSA is based on the number of respiratory sleep disruptions per hour of sleep during a sleep study, also called the apnea-hypopnea index (AHI). Basically, the higher the AHI, the more severe the sleep apnea. Most population studies suggest that about 60% of people with OSA fall into the mild category. In general, many studies demonstrate a linear relationship between the AHI and adverse health outcomes, lending strong support for treatment of moderate and severe OSA, but with less clear-cut support for clinical and/or cost-effective benefits for treating mild OSA.
Regardless of the criteria for categorizing OSA as mild, moderate, or severe, the severity of disease does not always correlate with the extent of symptoms. In other words, some people with very mild disease (based on their AHI) can be extremely symptomatic, with excessive sleepiness or severe insomnia, while others with severe disease have subjectively good sleep quality and do not have significant daytime impairment.
Sleep disorders also tend to overlap, and patients with OSA may suffer from comorbid insomnia, circadian (internal body clock) disorders, sleep movement disorders (like restless legs syndrome), and/or conditions of hypersomnia (such as narcolepsy). To truly improve a patient’s sleep and daytime functioning, a detailed sleep related history is needed, and sleep issues must be addressed via a comprehensive, multidimensional, and individualized approach.
When sleep apnea is moderate or severe, continuous positive airway pressure (CPAP) is considered the first-line treatment, and is the recommended treatment by the American Academy of Sleep Medicine (AASM). CPAP, by eliminating snoring, breathing disturbances, and drops in oxygen saturation, can essentially normalize breathing during sleep. However, to be most beneficial, CPAP should be worn consistently throughout sleep. Unfortunately, many studies of OSA set a relatively low bar for treatment adherence (many use a four-hour-per-night threshold), and do not necessarily take into account treatment efficacy (whether sleep apnea and related daytime symptoms persist despite treatment).
There have not always been consistent outcomes data or consensus about treatment recommendations for people with mild sleep apnea. Nonetheless, there are several studies that have demonstrated quality of life benefits in treating mild OSA, including a recent study published in The Lancet, where researchers from 11 centers throughout the United Kingdom recruited and randomized 301 patients with mild OSA to receive CPAP plus standard of care (sleep hygiene counselling) vs. standard of care alone, and followed them over three months. The results found that in patients with mild OSA, treatment with CPAP improved their quality of life, based on a validated questionnaire.
This study supports a comprehensive approach to evaluation and treatment of mild OSA. While all people with mild OSA may not need to be treated with CPAP, there are patients who can greatly benefit from it.
When sleep apnea is mild, treatment recommendations are less clear-cut, and should be determined based on the severity of your symptoms, your preferences, and other co-occurring health problems. Working in conjunction with your doctor, you can try a stepwise approach — if one treatment doesn’t work, you can stop that and try an alternative. Managing mild sleep apnea involves shared decision-making between you and your doctor, and you should consider just how bothered you are by sleep apnea symptoms, as well as other components of your health that could be made worse by untreated sleep apnea.
Conservative approaches for mild OSA:
If you have bothersome symptoms related to OSA — such as loud, disruptive snoring, long pauses in breathing, repeated nighttime awakenings, unrefreshing sleep, insomnia, trouble thinking, or excessive daytime sleepiness — or significant health problems that might be exacerbated by OSA (even mild) — such as arrhythmia, high blood pressure requiring multiple medications to control, stroke, or a severe mood disorder — medical treatment(s) for OSA should be considered.
The medical treatments for mild OSA:
Based on your symptoms, exam, and risk factors, your doctor may recommend a sleep study, or you might be referred to see a sleep medicine specialist. A comprehensive sleep assessment is needed to accurately evaluate sleep complaints, since sleep disorders tend to overlap. Treatment for mild OSA may improve sleep-related symptoms and your quality of life. However, there is no one-size-fits-all approach when it comes to sleep disorders, but rather a multidimensional and individualized approach to find what works for you.
The post Treating mild sleep apnea: Should you consider a CPAP device? appeared first on Harvard Health Blog.