Health & Fitness

A new cult favourite yoga brand has been doing the rounds on Instagram, and we're here to give you the lowdown on why everyone's so obsessed. And which pieces to get your hands on first.

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Periods can feel like strange and mysterious things sometimes. While some of us experience them like clockwork, for others they can be sporadic or even non-existent. Dr May Gilbert explains why isolation may have turned your menstrual cycle upside. 

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Need some motivation to stay on healthy bandwagon? Three inspiring Australian women share how they lost a combined 36 kilograms while at home. But the most incredible part about their transformations? The positive effect it had on their mindset and mood. 

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Iron is essential for hundreds of biological functions including DNA synthesis, oxygen transport and the use of energy. About 6% of the human body is iron and 25% of it is stored as ferritin.¹ Iron is used in every living thing. Plants, animals, bacteria and even cancer cells would not survive without iron.

Plants use it to make chlorophyll, while animals and humans need it to make hemoglobin in order to transport oxygen and carbon dioxide.² Your body recycles iron from red blood cells, and you can absorb it from your food. A common symptom of iron deficiency is anemia.³ However, anemia is not always present with iron deficiency in children.

Since it is needed for cognitive development and to establish normal behavioral patterns, deficiency in children may present as poor school performance. There is limited evidence that using supplementation can improve the damage done by deficiency in young children.

However, what many people don't realize is that iron overload is more common than iron deficiency, and that it can trigger significant health problems, including cancer and death. Your body has a limited ability to excrete iron, so it can build up in your pancreas, liver and heart.

Too Much Iron Affects Joints and Metabolism

Since iron is found throughout your body, an abundance can create significant health conditions in multiple systems. In one study,⁴ researchers found that excess iron in individuals with metabolic syndrome affected their blood pressure and other markers of cardiovascular risk, as well as glycemic control.

The researchers engaged 64 individuals who had a diagnosis of metabolic syndrome. They were randomly assigned to one of two groups. In the first, participants gave blood at the beginning of the study and after four weeks. The amount of blood removed was dependent on each individual's iron levels.

The researchers were looking for a change in systolic blood pressure and insulin sensitivity, as well as hemoglobin A1c, plasma glucose, heart rate and blood lipids. They found a significant reduction in systolic blood pressure in the group who gave blood at the beginning and end of the study.

There was no significant effect on insulin sensitivity, but the participants who gave blood had lower blood glucose levels, hemoglobin A1c and heart rate.

In another study⁵ scientists evaluated the result of removing blood in individuals who had chronic gout. They enrolled 12 people with hyperuricemia and removed some of their blood over a period of 28 months in order to maintain their body at the lowest amount of iron stores possible, without inducing anemia.

During the study, they saw that participants had a marked reduction in the number and severity of gout attacks. Removing blood was found to be safe and beneficial.

Overload Is More Common Than Deficiency

Iron is also a common nutritional supplement. Since it's added to many multivitamins and mineral supplements, it's easy to get too much. Many processed foods are also fortified with iron. For instance, two servings of fortified breakfast cereal may provide you with as much as 44 mg,⁶ bringing you dangerously close to the upper tolerance limit of 45 mg for adults.

This is well over the recommended daily allowance, which is 8 mg for men and 18 mg for premenopausal women.⁷ Since the body excretes only small amounts, nearly all adult men and postmenopausal women are at risk for overload and many doctors don't appreciate the importance of checking for it. Women, who lose blood regularly during their menstrual period, do not have the same risk.

Another factor contributing to the possibility of iron overload is hemochromatosis.⁸ This is one of the most prevalent genetic conditions in Americans. It impairs the body's iron regulation, which means that those who have it tend to absorb higher amounts than normal.

It takes two inherited copies of the genetic mutation, one from your mother and one from your father, to cause the disease. Results from one study were used to estimate that 40% to 70% of those with the defective genes develop clinical evidence of iron overload.⁹

Another common cause of iron excess is the regular consumption of alcohol.¹⁰ This increases the amount of iron you absorb from your diet. In other words, if you drink alcohol with foods high in iron, you will likely absorb more than you need.

Other contributors may include cooking in iron pots and pans, eating processed foods, drinking well water that's high in iron and using multiple vitamins and mineral supplements together.

Severe Blood Shortages Another Consequence of COVID-19

Blood donation is one of the easiest ways to reduce your ferritin level and iron overload. It promotes your good health and may save the life of someone else. Unfortunately, the American Red Cross had to cancel nearly 2,700 blood drives across the country when people began practicing social distancing due to regulations related to SARS-CoV-2.¹¹

This led to severe shortages and has resulted in 86,000 fewer donations. The Red Cross collects blood at various permanent locations and during blood drives at workplaces, college campuses and schools.

More than 80% of the blood they collect comes from blood drives. While they're adding donation slots to improve opportunities to give, blood availability remains low. Chris Hrouda, president of the Red Cross Biomedical Services, voiced concerns over the shortage to a reporter with the Press Herald:¹²

"In our experience, the American public comes together to support those in need during times of shortage and that support is needed now more than ever during this unprecedented public health crisis. Unfortunately, when people stop donating blood, it forces doctors to make hard choices about patient care, which is why we need those who are healthy and well to roll up a sleeve and give the gift of life.

We know that people want to help, but they may be hesitant to visit a blood drive during this time. We want to assure the public that blood donation is a safe process, and we have put additional precautions in place at our blood drives and donation centers to protect all who come out."

To donate, you only need a blood donor card, a driver's license or two forms of identification. People who are at least 17, weigh at least 110 pounds and are in generally good health are eligible.

Why Too Much Iron Can Be Dangerous

At the cellular level, iron can react with hydrogen peroxide in the inner mitochondrial membrane.¹³ This is a normal part of cellular aerobic respiration. However, excess iron catalyzes the formation of too many damaging hydroxyl free radicals from peroxide.

This is one pathway that can accelerate chronic disease. In addition, research¹⁴ also shows that excessive iron promotes apoptosis and ferroptosis in cardiomyocytes. Ferroptosis is cell death that is dependent on and regulated by iron.¹⁵ The cardiomyocytes generate and control contractions. Apoptosis is programmed cell death of diseased and worn-out cells.

Too much iron can impair your heart function through mitochondrial abnormalities and the death of muscle cells in your heart. Iron overload is also a concern in Alzheimer's disease.¹⁶ The buildup of iron increases oxidative stress, which has a "rusting effect" in your brain, commonly found in Alzheimer's patients.¹⁷

Other researchers suggest that iron in the cerebrospinal fluid is strongly correlated with Alzheimer's and a particular risk allele, APOE-ε4.¹⁸ Thus far, conventional treatment has been focused on clearing amyloid proteins in the brain. While the approach appeared logical, there has been limited success.

Evidence now suggests reducing excess iron may be an effective way of slowing or preventing Alzheimer's disease. Read more about this in "How Excess Iron Raises Your Risk for Alzheimer's."

GGT: A Predictor of Iron Toxicity and Mortality

A second measurable factor with an impact on iron toxicity and mortality is gamma glutamyl transpeptidase, sometimes called gamma-glutamyl transferase (GGT). This is a liver enzyme involved in the metabolism of glutathione and the transport of amino acids and peptides.¹⁹ In this video interview with Gerry Koenig we discuss GGT, the value of measuring GGT and why it's so important to your health.

GGT can be used as a screening marker for excess free iron, liver damage and as an indicator of your risk of sudden cardiac death and chronic kidney disease.²⁰ In recent years, researchers have discovered GGT interacts with iron. Low levels tend to be protective against high levels of ferritin.

This means, if your GGT is low, you have some protection even when your ferritin levels are a little higher than ideal. However, when both serum ferritin and GGT are high it represents an increased risk of chronic health problems and early death. Even when ferritin levels are low, an elevated GGT needs to be addressed.

While the test is often used as a marker for alcohol-related liver disease, the predictive value also applies to diabetes, metabolic syndrome, cardiovascular disease and all-cause mortality.²¹ GGT may also be used as an early marker for atherosclerosis, arterial stiffness, gestational diabetes and a variety of liver diseases, including viral hepatitis.

Test Iron and GGT Levels and Reduce Them to Normal

As with many lab tests, the normal ranges will vary between laboratories and are often far from ideal and the normal ranges used for GGT may not be adequate to prevent disease. As I've shared before, the range of ideal to "normal" GGT can be wide. Koenig's suggestions, which are in the ranges of what Mayo Clinic suggests,²² are below:

	Ideal GGT Level, units per liter (U/L)	Average level, above which risk for chronic disease increases significantly	"Normal" GGT Levels
Men	< 16 U/L	25 U/L	Up to 70 U/L
Women	< 9 U/L	18 U/L	Up to 45 U/L

To determine your healthy ranges, you'll need both your ferritin and GGT levels tested. According to Koenig, women who have a GGT level above 30 units per liter (U/L) have a higher risk of cancer and autoimmune disease. While other tests have a broad range between what's healthy and what's risky, the range for GGT between health and disease is in the single digits.²³

"Part of it is dependent on body weight," Koenig says. "Strangely enough, the most recent indications are that people who are too thin (whatever their level of GGT is), it could be harmful if [their GGT is] relatively high. For instance, for a thin woman with a GGT … in the range of the second quartile, which is going to be generally 14 to 18 today it can be dangerous if she's expecting to have children and has a very low BMI."

Ideal ferritin levels for adult men and non-menstruating women is between 30 nanograms per milliliter (ng/ml) to 60 ng/ml. Some labs use a normal range of 200 to 300 ng/ml, which is far too high for optimal health. Ideally, I believe you don't want to drop below 20 ng/ml or above 80 ng/ml.

As demonstrated in the research studies above, it's easy to lower your iron levels by donating blood to two or three times a year. In the past, that is how I maintained ferritin levels below 100 ng/ml.

However, once I started a comprehensive detoxification strategy using near and far infrared sauna, my ferritin levels continued to drop without giving blood. An effective detoxification program can also lower GGT levels.

GGT is inversely related to glutathione. This means as your GGT level rises, your glutathione goes down, which is one way an elevated GGT can harm your health. You also can lower your GGT levels by reducing or eliminating alcohol, carefully considering your protein intake and raising the amount of fruits and vegetables you eat.

However, by elevating glutathione, you lower your GGT. The amino acid cysteine plays an important role in the production of glutathione and can be found in whey protein, poultry and eggs. Red meat and alcohol will raise your GGT levels.²⁴

Certain medications can also raise your GGT. Speak with your pharmacist to determine if any over-the-counter medication or prescription drugs you are taking may have an impact and confer with your doctor to see if you can stop or switch to something else.

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Bartering and the exchange of currency have long and interesting histories. We've gone from trading products and metal coins to exchanging paper notes and now cryptocurrency, based on digital encryption. While it might seem that cryptocurrency is a natural next step in financial evolution, remember that just because something is possible doesn't mean it's better.

Bitcoin was the first established cryptocurrency to hit the market.¹ It is based on an online "currency" secured through encryption. The first hint of it arrived in 2008 in a paper posted to a mailing list by someone using the name Satoshi Nakamoto. No one knows who that person really is (or was), even today.

The software went public in 2009 and the first exchange happened in 2010 when someone traded 10,000 Bitcoins for two pizzas. According to Forbes Magazine, had the individual exchanging those Bitcoins kept them, the value would have jumped to $100 million in 2017.

But, long before that, back in 2013 the price of one coin dropped from $1,000 to $300. This was likely triggered by a six-hour period during which there were two digital networks, with two transaction histories, operating at the same time.² This glitch cost Bitcoin's value to drop for more than two years before it recovered.

One of the largest thefts of Bitcoin occurred in January 2014. Mt.Gox, a cryptocurrency exchange, was hacked and 850,000 Bitcoins valued at $450 million were stolen. As cryptocurrencies have continued to be exchanged, Google, Gates and several partners recently revealed a new level of global digital currency and money transfer.

Mojaloop Foundation Aiming at a Global Currency

The history of Mojaloop began in Toronto in 2017 when the Bill & Melinda Gates Foundation started an open-source banking project.³ Since then, interest has varied. In 2019, The Gates Foundation backed DFS Lab to hold a hackathon with the intent of introducing the Mojaloop software to tech companies.

Jake Kendall, executive director for DFS Lab, spoke to a reporter at Forbes, excited about the possibilities Mojaloop may present to undeveloped countries: "We see Majaloop [sic] as part of [a] bigger trend toward standards-based interoperability and improved interlinking in financial services."

Kendall was employed in financial development at the Gates Foundation before moving to DFS Lab. Nearly one year later, Google and the Gates Foundation announced a coalition of nonprofit and tech companies to form the Mojaloop Foundation.

Some of the companies included the Rockefeller Foundation, Coil, the Omidyar Network and ModusBox.⁴ The rollout in 2020 is a culmination of testing what works in digital currency with the goal of repeating outcomes of a similar digital platform used in Kenya, called M-Pesa⁵ with an aim at serving 1.7 billion people.⁶

The M-Pesa platform was introduced in 2007 and by 2012 had 17 million accounts. The software allows a "monetary value to be stored on a mobile phone and sent to other users via text messages."⁷ Monetary efficiency, in an area of the world where most people don't have access to banks, may have helped 194,000 households get out of poverty.

The technology is just the beginning. David Wexler, CEO of ModusBox, told Fortune Magazine that the system will require the ability to connect across country borders and ensure the tool is accessible to those who need a means of connecting with digital financial services.

To that end, the Mojaloop Foundation plans to provide experts within the countries to help develop solutions and guide governmental policies. It's intended to be managed by the country's government or financial authorities, but the sharing standard means it becomes interoperable across borders.

What this means is the system will be able to work with, or use parts of, another system within the country. The Mojaloop Foundation describes their platform this way:⁸

"Whole, adapted, or as a blueprint — the Mojaloop Foundation's open source software can be used by organizations to build interoperable, digital payment systems that enable seamless, affordable financial services between individual users, banks, government entities, merchants, mobile network operators, providers, and technology companies — connecting the underserved with the emerging digital economy."

Cryptocurrency Has Always Been Fundamentally Decentralized

Globally, nearly 25 million people use Bitcoin.⁹ The foundation in cryptocurrency is that the process is peer-to-peer. In other words, it is decentralized and does not work with a bank or a credit card. The process is controlled solely by users as opposed to a central bank or a government.

Cryptocurrencies are developed for a variety of reasons. For instance, Bitcoins are used to buy and sell products and services. However, some companies are using cryptocurrency to give buyers access to a product or service that the company is offering or plans to offer.¹⁰

It is a way of raising money. But, unlike stock where you own part of the company that's offering it, during an initial coin offering (ICO) you are buying a future service or product.

According to CoinMarketCap, there are more than 5,500 different cryptocurrencies currently on the market with a total net worth of $246.48 billion.¹¹ Initially, cryptocurrency is purchased using cash. This can then be exchanged for goods and services using a digital platform through a cryptocurrency wallet.¹²

To send money across the world, some platforms use a protocol called Interledger,¹³ which allows a person to conduct transactions across various forms of currency. Each cryptocurrency maintains a ledger, often secured through a blockchain or digital public ledger. The transactions are encrypted to prevent hacking.

The backbone of cryptocurrency systems is meant to be decentralized. However, while Mojaloop-based systems currently use fiat currency (money established by a government and not backed by intrinsic value such as gold or silver) or cryptocurrency, it is intended to be hosted by a government or financial authorities.¹⁴

Whether governments will allow the system to remain decentralized after initiation cannot be determined. Rodger Voorhies from the Gates Foundation believes that the expansion of a fast-payment infrastructure, such as Mojaloop, can only help during pandemic situations.

The Major Players: Gates, Google and Ripple

Mojaloop is poised to create a platform that allows people from all over the world to send money to each other with low transaction fees. It allows countries, financial institutions and developers to make changes to their own platform and share upgrades.

The initiative is designed to address the needs of rural populations, allowing them access to digital payments through their smartphones. The platform also has other functions that give users the ability to access financial markets. The software creation was intended to engage banks, governments, regulatory agencies and others in developing markets to provide services for those without access to a bank.¹⁵

Yet, doing so may ultimately backfire. With Google's history of tracking personal information and Gates' apparent desire to influence personal choice, it's difficult to imagine their focus will change.

Another founding member is Ripple, which is both a processing platform and a cryptocurrency.¹⁶ In 2015 the group partnered with Santander Bank, one of the largest banks in Europe. This quickly drove up the value of their cryptocurrency, XRP.¹⁷

During the announcement, Ripple's representative shared that the company was planning work to achieve the vision of the Internet of Value. Under this concept, actual value is transferred from peer-to-peer and not through an intermediary such as a bank or credit card company.

Unlike other cryptocurrencies that rely on blockchain to encrypt and safeguard the transactions, Ripple uses a patented technology called Ripple protocol consensus algorithm (RPCA). Included in their network called RippleNet are several institutional payment providers that people use to send money around the world.

These providers include American Express, PNC Bank, Interbank and MoneyGram.¹⁸ Together with Google, Gates and other large tech companies in the coalition, Ripple is positioned to potentially gain control of a created global currency and drive down the value of country-based currency.

Facebook and Yahoo! Create Their Own Exchange

While Google, Gates, Ripple and the Rockefeller Foundation have their eye on a global currency system, other large tech companies are scrambling to claim their own piece of the digital pie. Amid Congressional scrutiny over the sale and misuse of their consumers' personal data, Facebook registered Libra Networks in Geneva, Switzerland, in 2019.¹⁹

Facebook Global Holdings is the stakeholder for a company that will focus on "investing, payments, financing, identity management, analytics, big data, blockchain and other technologies."

When Facebook registered Libra, it had more than 2 billion users. It also owned Instagram, Messenger and WhatsApp that each boasted more than 1 billion users. Their stated mission is a "simple global payment system and financial infrastructure."²⁰

Yet, as 2019 came to a close, Facebook wasn't enjoying the appreciation they may have hoped to generate.²¹ Instead, they lost eight of their founding members and took criticism from legislators who questioned the potential fallout from linking a payment system to a company whose privacy track record is less than stellar.

Before the launch of Libra Networks was announced, the U.S. Senate Committee on Banking, Housing and Urban Affairs²² wrote to Facebook founder Mark Zuckerberg with a list of specific concerns after learning through an article in the Wall Street Journal that:

"… Facebook is recruiting dozens of financial and online merchants to help launch a cryptocurrency-based payments system using its social network … In addition, privacy experts have raised questions about Facebook's extensive data collection practices and whether any of the data collected by Facebook is being used for purposes that do or should subject Facebook to the Fair Credit Reporting Act."

By October 2019,²³ Paypal, Mastercard, Visa, Stripe and eBay had left the fold. Libra also lost the online payment platform MercadoPago and Booking Holdings, which runs Priceline, Kayak and OpenTable. In February 2020, they acquired Shopify and another cryptocurrency start up.²⁴

By April 2020, Libra had pivoted. Facebook organized an independent group, Libra Association, that announced a plan to offer coins backed by one currency. This is in addition to those currently offered that are backed by multiple currencies. This was the result of global governmental oversight unwilling to work with the privacy-troubled company.²⁵

Not to be left behind, Yahoo! has a 40% share in Taotao, a cryptocurrency exchange that recorded a 200% rise in new accounts last year.²⁶ Growing movement in the digital financial space may mean the cost of cryptocurrency will rise.

However, more importantly is the potential for large technology companies and the billionaire owners to assemble greater wealth and power by integrating their platforms and software in a market aimed at the global economy and hosted by governments and financial institutions.

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Is the COVID-19 pandemic the result of a manmade virus? And, if so, what does that say about mankind's ability to safely conduct gain-of-function experiments? "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.¹

In reality, this kind of research does not appear to have improved governments' pandemic responses at all. If anything, it's a curious coincidence that the very viruses undergoing gain-of-function research are the ones causing pandemics.

As noted in the 2016 paper,² "Gain-of-Function Research: Ethical Analysis," even if gain-of-function research does lead to improved and effective control measures, laboratory accidents or "malevolent action" in which souped-up pathogens are released can still result in casualties numbering in the millions.

The Controversy Surrounding Gain-of-Function Research

Gain-of-function research has been controversial since it started being openly discussed.³ As noted in the 2012 paper, "Rethinking Biosafety in Research on Potential Pandemic Pathogens":⁴

"If accidentally released, mammalian-transmissible influenza A/H5N1 viruses could pose a greater threat to public health than possibly any other infectious agent currently under study in laboratories, because of such viruses' likely combination of transmissibility and virulence to humans …

Such potential pandemic pathogens, as they have been called, jeopardize not only laboratory workers and their contacts, but also the wider population, who should be involved in assessments of when such risks are acceptable in the service of scientific knowledge that may itself bear major public health benefits."

The U.S. put a moratorium⁵ on government funding of gain-of-function research into SARS, MERS and avian flu in 2014, following several biosafety lapses at federal research facilities.⁶ In a May 2016 paper in The Journal of Infectious Diseases, American scientists noted:⁷

"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."

Again and again, scientists have called for public transparency, saying the public should be part of the decision process, seeing how our health is at stake and it's our taxpayer money that's being used to conduct this research.

As noted in a 2013 paper,⁸ "controllability of escape events is not guaranteed and, given the rapid increase of biosafety laboratories worldwide, this poses a serious threat to human health."

Funding Pause Didn't Halt All Gain-of-Function Research

Twenty-one gain-of-function research projects were placed on hold when funding was paused,^9,10 but several were given special permission to continue,¹¹ including experiments on bat coronaviruses¹² at the Wuhan Institute of Virology in China, funded by the National Institute of Allergy and Infectious Diseases (NIAID), under Fauci's leadership.

As noted in "A SARS-Like Cluster of Circulating Bat Coronaviruses Shows Potential for Human Emergence," published in Nature Medicine in 2015 by Shi Zhengli-Li et.al.:¹³

"These studies were initiated before the U.S. Government Deliberative Process Research Funding Pause on Selected Gain-of-Function Research Involving Influenza, MERS and SARS Viruses. This paper has been reviewed by the funding agency, the NIH. Continuation of these studies was requested, and this has been approved by the NIH."

Near the end of 2017, the moratorium was lifted,¹⁴ and new guidelines¹⁵ and review processes for gain-of-function research were issued but not made mandatory. According to a January 2020 Nature article,¹⁶ researchers are now pushing for greater public transparency when it comes to government's funding of gain-of-function research. Whether or not that will actually happen remains to be seen:

"U.S. disease researchers are pushing the government to be more transparent about federally funded research that involves making pathogens more deadly or more transmissible.

Several disease researchers who attended a recent meeting to discuss transparency around such studies say the U.S. government should offer a public explanation when it approves such 'gain-of-function' experiments, disclose who made the decision to fund them and make a broad public announcement when a study begins. Others argued that greater transparency could make it harder to approve necessary research.

The debate over how much to disclose about such work is revving up because the government is preparing to revisit rules that guide gain-of-function research — especially with regard to their communication to the public."

SARS-CoV-2 — Engineered or Not?

Because of the heavily censored media, any quick online search will easily lead you to believe that there's no evidence of SARS-CoV-2 being an engineered virus, but mounting evidence points directly to that being a reality.

What some experts point to as "smoking gun" evidence for it being a manmade virus are the Antiviral Research paper,¹⁷ "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,"^18,19 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.^20,21

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's²² and Yuri Deigin's²³ reviews of these findings in "The Smoking Gun Proving SARS-CoV-2 Is an Engineered Virus."

Logic Behind Manmade Claims

An anonymous — possibly Chinese — researcher has also discussed the scientific evidence supporting the claim that SARS-CoV-2 is a manmade virus in a blog called Nerd Has Power. The anonymous blogger, who refers to him or herself as "a nobody scientist,"²⁴ points out there appears to be a concerted effort to promote the idea that SARS-CoV-2 is a natural occurrence.

"Not nearly as much literature or other forms of substantial writing have been put out to describe or argue for the other possibility — this virus is man-made," the blogger states in a March 15, 2020, post.²⁵

He or she then goes on to explain the importance of the S1 and S2 spike sections of a given virus, and details significant changes found in the S1 portion of the SARS-CoV-2 spike protein, "which dictates which host a coronavirus targets." According to the blogger:²⁶

"… the details of these differences and the way the human and the bat viruses differ from each other here in S1, in my and many other people's eyes, practically spell out the origin of the Wuhan coronavirus — it is created by people, not by nature."

The reason people are suspicious of the origin of SARS-CoV-2, the blogger states, is in large part due to the virus' genome, i.e., its genetic sequence, compared to related coronaviruses. While genetic sequences can be compared using either gene sequences or protein sequences, when it comes to viruses, the sequence you choose makes little difference, as the entire genome "is practically translated into proteins."

Using the protein sequence for his or her comparison, the blogger explains that since SARS-CoV-2 is only 86% identical to the SARS coronavirus, it could not have evolved from SARS. Yet, it's oddly similar to the bat coronaviruses ZC45 and ZXC21, sharing 95% of the genome of either of these two, and certain proteins are 100% identical.

"The nucleocapsid is 94% identical. The membrane protein is 98.6% identical. The S2 portion (2nd half) of the spike protein is 95% identical. However, when it comes to the S1 portion (1st half) of the spike protein, the sequence identity suddenly drops to 69%.

This pattern of sequence conservation, between either of the closely related bat coronaviruses and the Wuhan coronavirus, is extremely rare and strange!" the blogger states, adding:²⁷

"This is extremely rare because natural evolution typically takes place when changes (mutations) occur randomly across the whole genome. You would then expect the rate of mutation being more or less the same for all parts of the genome."

SARS-CoV-2 Unlikely To Be the Result of Recombination

While an evolutionary event known as recombination can account for this discrepancy, the blogger explains why recombination is "practically impossible" in the case of SARS-CoV-2:²⁸

"Importantly, to go from such ancestor to the Wuhan coronavirus, one combination event is not enough. What has to happen is that recombination has to take place twice during the evolution of the Wuhan coronavirus.

In one occasion, the ancestor bat coronavirus would have to acquire, through recombination with a SARS-like coronavirus, the precise short segment of S1 that is responsible for human ACE2 interaction …

In another occasion, the 'improved' bat coronavirus would further swap in a furin-cleavage site through recombination with yet another coronavirus that carries a furin-cleavage site between its S1 and S2 of spike.

Also, again, given the overall high sequence identity (95%) between the bat coronaviruses and the Wuhan coronavirus, it is reasonable to believe that these two diverged from each other fairly recently. Therefore, both recombination events must have taken place fairly recently as well.

Now, we know that SARS crossing over to infect human is a very rare event. To have another SARS-like sequence exist in nature so that the ancestor bat coronavirus can do recombination with is a very unlike event.

Not to mention that this SARS-like virus must have a spike that binds ACE2 the same way as SARS and yet the piece of S1 that is most critical for binding ACE2 would differ with that of SARS spike only at non-essential sites.

On top of that, furin-cleavge site has not been observed in any beta coronaviruses in the same lineage so far. Although similar furin-cleavage sites have been observed in other coronaviruses, none of them contains the same exact sequence.

Therefore, the chance that the furin-cleavage site in the Wuhan coronavirus was obtained through recombination with another furin-cleavage-site-containing coronavirus is very low. Now, what are chances for both of these next-to-impossible recombination events to take place? My answer is NO CHANCE."

S1 Spike Portion Has Undergone Strange Changes

As explained in "The Smoking Gun Proving SARS-CoV-2 Is an Engineered Virus," (hyperlinked earlier), viruses use a two-step process to gain entry into your cells. First, the S1 portion of the spike protein must bind to an ACE2 receptor.

Next the S2 subunit must be proteolytically cleaved (cut). Without this protein cleavage, the virus would simply attach to the receptor and not get any further. Furin is one of the enzymes that can do that.

Discussing the S1 portion of the spike, the part responsible for the virus' ability to bind to the host receptor (in this case the ACE2 receptor), the blogger notes:²⁹

"Whether or not a particular 'lock' can be opened by a specific 'key' is decided exclusively by this S1 part of spike. In other words, S1 of a coronavirus dictates which host(s) or cells the virus can infect. Now you may be able to appreciate what I call extremely strange.

While everything else of the Wuhan coronavirus remains almost identical to the two bat coronaviruses, the S1 portion, which dictates which host a coronavirus targets, has changed significantly from the two bat coronaviruses to the Wuhan coronavirus."

The following graphic shows the genetic sequence of SARS-CoV-2's spike proteins compared to five other relevant coronaviruses, including the Wuhan-Hu-1 virus, isolated from the current pandemic, along with 2019-nCov_USA-AZ1. The remaining four are two bat coronaviruses and two SARS coronaviruses.

The horizontal orange lines demarcate the segment that determines the viruses' ability to interact with the human ACE2 receptor. The green lines indicate the furin-cleavage site that is only found in the coronaviruses isolated during the current pandemic.

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According to the blogger:³⁰

"The Wuhan coronavirus, while being almost identical to their bat relatives (ZC45 and ZXC21) everywhere else, has somehow 'inherited' the critical, short piece from SARS spike to replace the incompetent piece in the bat coronavirus spike.

As a result of this miraculous 'replacement' in S1 — all key residues preserved and many non-essential residues changed, the Wuhan coronavirus has practically 'acquired' the ability to infect humans, something its closest bat relatives do not have. Could natural evolution achieve something this precise and, at the same time, this deceptive? …

Let's move on to appreciate magic trick #2. Please look at the region marked by two green lines … Here only the Wuhan coronaviruses contain an additional piece, SPRRA.

Importantly, this added piece allows the spike protein to be readily cleaved by a host protease enzyme — furin, a desirable property known to produce more infectious viruses in the case of influenza. Note that no beta coronaviruses in the same lineage … except this new Wuhan coronavirus, contain such a furin-cleavage site."

No Proof SARS-CoV-2 Emerged Naturally

According to a 2020 paper³¹ in the journal Nature Medicine, "The Proximal Origin of SARS-CoV-2," the virus is the result of natural mutation and selection in bats, pangolins and/or human hosts.

The authors claim two key characteristics of the virus as evidence of natural evolution: the absence of a previously used virus backbone, and the slightly imperfect way in which the virus binds to human cells.

Based on computer modeling data, the virus is not perfectly constructed, and this, they claim, is "strong evidence that SARS-CoV-2 is not the product of purposeful manipulation." In other words, their argument is that scientists would have followed the sequences indicated by computer modeling, and since the virus doesn't have the computer predicted amino acid sequence, it must have arisen spontaneously. A May 20, 2020, GM Watch article³² points out:

"However, the London-based molecular geneticist Dr. Michael Antoniou commented that this line of reasoning fails to take into account that there are a number of laboratory-based systems that can select for high affinity RBD variants that are able to take into account the complex environment of a living organism.

This complex environment may impact the efficiency with which the SARS-CoV spike protein can find the ACE2 receptor and bind to it. An RBD selected via these more realistic real-world experimental systems would be just as 'ideal,' or even more so, for human ACE2 binding than any RBD that a computer model could predict.

And crucially, it would likely be different in amino acid sequence. So the fact that SARS-CoV-2 doesn't have the same RBD amino acid sequence as the one that the computer program predicted in no way rules out the possibility that it was genetically engineered."

Undetectable Methods of Genetic Engineering Have Been Used

GM Watch also highlights Dr. Richard Ebright's critique of that Nature Medicine paper. Ebright, an infectious disease expert at Rutgers University, points out that U.S. and Chinese researchers have genetically engineered bat coronaviruses using methods that "leave no sign or signature of human manipulation." According to GM Watch:³³

"Ebright flagged up a scientific paper³⁴ published in 2017 by WIV [Wuhan Institute of Virology] scientists, including Shi Zhengli, the virologist leading the research into bat coronaviruses, working in collaboration with Peter Daszak of the U.S.-based EcoHealth Alliance.

Funding was shared between Chinese and U.S. institutions, the latter including the U.S. National Institutes of Health and USAID. The researchers report having conducted virus infectivity experiments where genetic material is combined from different varieties of SARS-related coronaviruses to form novel 'chimeric' versions.

This formed part of their research into what mutations were needed to allow certain bat coronaviruses to bind to the human ACE2 receptor — a key step in the human infectivity of SARS-CoV-2. The WIV scientists did this, Ebright points out, 'using 'seamless ligation' procedures that leave no signatures of human manipulation.'"

Interestingly, "The Proximal Origin of SARS-CoV-2,"³⁵ does not include seamless ligation in its review of genetic engineering methods that could have been used. This, despite the fact that researchers experimenting with bat coronaviruses at WIV were using this very method.

Equally interesting is Daszak's comments in the video above about how over 100 SARS coronaviruses have been found, some of which can enter human cells and cause disease in human mouse models — and are untreatable and cannot be protected against with vaccines!

"A group of scientists from the University of North Carolina in the USA, with the WIV's Shi Zhengli as a collaborator, published a study³⁶ in 2015 describing similar experiments involving chimeric coronaviruses, which were also created using standard undetectable genetic engineering techniques," GM Watch writes.³⁷

"Commenting on Andersen and his team's omission of these methods from their article³⁸ in Nature Medicine, Dr. Antoniou told us, 'This shows that these authors' conclusions about whether genetic engineering could have been involved are not justified by the available evidence.'"

Antoniou tried submitting a letter to Nature Medicine pointing out these omissions, but the journal refused to publish it, saying his counterarguments don't advance or clarify understanding of the original article. You can find Antoniou's letter at the bottom of GM Watch's article.³⁹

Yet another way you can alter a virus in a laboratory — without genetic engineering — is by culturing the virus in cells that have the human ACE2 receptor.

Over time, the virus can thereby adapt and gain the ability to bind to that receptor. This technique, highlighted by Nikolai Petrovsky, a researcher at the College of Medicine and Public Health at Flinders University in South Australia, was reviewed by Live Science in an April 18, 2020, article.⁴⁰

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