Health & Fitness

According to a study that examined how informed consent is given to COVID-19 vaccine trial participants, disclosure forms fail to inform volunteers that the vaccine might make them susceptible to more severe disease if they’re exposed to the virus.

The study,¹ “Informed Consent Disclosure to Vaccine Trial Subjects of Risk of COVID-19 Vaccine Worsening Clinical Disease,” published in the International Journal of Clinical Practice, October 28, 2020, points out that “COVID-19 vaccines designed to elicit neutralizing antibodies may sensitize vaccine recipients to more severe disease than if they were not vaccinated.”

“Vaccines for SARS, MERS and RSV have never been approved, and the data generated in the development and testing of these vaccines suggest a serious mechanistic concern: that vaccines designed empirically using the traditional approach (consisting of the unmodified or minimally modified coronavirus viral spike to elicit neutralizing antibodies), be they composed of protein, viral vector, DNA or RNA and irrespective of delivery method, may worsen COVID-19 disease via antibody-dependent enhancement (ADE),” the paper states.

“This risk is sufficiently obscured in clinical trial protocols and consent forms for ongoing COVID-19 vaccine trials that adequate patient comprehension of this risk is unlikely to occur, obviating truly informed consent by subjects in these trials.

The specific and significant COVID-19 risk of ADE should have been and should be prominently and independently disclosed to research subjects currently in vaccine trials, as well as those being recruited for the trials and future patients after vaccine approval, in order to meet the medical ethics standard of patient comprehension for informed consent.”

What Is Antibody-Dependent Enhancement?

As noted by the authors of that International Journal of Clinical Practice paper, previous coronavirus vaccine efforts — for severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and respiratory syncytial virus (RSV) — have revealed a serious concern: The vaccines have a tendency to trigger antibody-dependent enhancement.

What exactly does that mean? In a nutshell, it means that rather than enhance your immunity against the infection, the vaccine actually enhances the virus’ ability to enter and infect your cells, resulting in more severe disease than had you not been vaccinated.²

This is the exact opposite of what a vaccine is supposed to do, and a significant problem that has been pointed out from the very beginning of this push for a COVID-19 vaccine. The 2003 review paper “Antibody-Dependent Enhancement of Virus Infection and Disease” explains it this way:³

“In general, virus-specific antibodies are considered antiviral and play an important role in the control of virus infections in a number of ways. However, in some instances, the presence of specific antibodies can be beneficial to the virus. This activity is known as antibody-dependent enhancement (ADE) of virus infection.

The ADE of virus infection is a phenomenon in which virus-specific antibodies enhance the entry of virus, and in some cases the replication of virus, into monocytes/macrophages and granulocytic cells through interaction with Fc and/or complement receptors.

This phenomenon has been reported in vitro and in vivo for viruses representing numerous families and genera of public health and veterinary importance. These viruses share some common features such as preferential replication in macrophages, ability to establish persistence, and antigenic diversity. For some viruses, ADE of infection has become a great concern to disease control by vaccination.”

Previous Coronavirus Vaccine Efforts Have All Failed

In my May 2020 interview above with Robert Kennedy Jr., he summarized the history of coronavirus vaccine development, which began in 2002, following three consecutive SARS outbreaks. By 2012, Chinese, American and European scientists were working on SARS vaccine development, and had about 30 promising candidates.

Of those, the four best vaccine candidates were then given to ferrets, which are the closest analogue to human lung infections. In the video below, which is a select outtake from my full interview, Kennedy explains what happened next. While the ferrets displayed robust antibody response, which is the metric used for vaccine licensing, once they were challenged with the wild virus, they all became severely ill and died.

The same thing happened when they tried to develop an RSV vaccine in the 1960s. RSV is an upper respiratory illness that is very similar to that caused by coronaviruses. At that time, they had decided to skip animal trials and go directly to human trials.

“They tested it on I think about 35 children, and the same thing happened,” Kennedy said. “The children developed a champion antibody response — robust, durable. It looked perfect [but when] the children were exposed to the wild virus, they all became sick. Two of them died. They abandoned the vaccine. It was a big embarrassment to FDA and NIH.”

Neutralizing Versus Binding Antibodies

Coronaviruses produce not just one but two different types of antibodies:

• Neutralizing antibodies,⁴ also referred to as immoglobulin G (IgG) antibodies, that fight the infection
• Binding antibodies⁵ (also known as nonneutralizing antibodies) that cannot prevent viral infection 

Instead of preventing viral infection, binding antibodies trigger an abnormal immune response known as “paradoxical immune enhancement.” Another way to look at this is your immune system is actually backfiring and not functioning to protect you but actually making you worse.

Many of the COVID-19 vaccines currently in the running are using mRNA to instruct your cells to make the SARS-CoV-2 spike protein (S protein). The spike protein, which is what attaches to the ACE2 receptor of the cell, is the first stage of the two-stage process viruses use to gain entry into cells.

The idea is that by creating the SARS-CoV-2 spike protein, your immune system will commence production of antibodies, without making you sick in the process. The key question is, which of the two types of antibodies are being produced through this process?

Without Neutralizing Antibodies, Expect More Severe Illness

In an April 2020 Twitter thread,⁶ The Immunologist noted: “While developing vaccines … and considering immunity passports, we must first understand the complex role of antibodies in SARS, MERS and COVID-19.” He goes on to list several coronavirus vaccine studies that have raised concerns about ADE.

The first is a 2017 study⁷ in PLOS Pathogens, ”Enhanced Inflammation in New Zealand White Rabbits When MERS-CoV Reinfection Occurs in the Absence of Neutralizing Antibody,” which investigated whether getting infected with MERS would protect the subject against reinfection, as is typically the case with many viral illnesses. (Meaning, once you recover from a viral infection, say measles, you’re immune and won’t contract the illness again.)

To determine how MERS affects the immune system, the researchers infected white rabbits with the virus. The rabbits got sick and developed antibodies, but those antibodies were not the neutralizing kind, meaning the kind of antibodies that block infection. As a result, they were not protected from reinfection, and when exposed to MERS for a second time, they became ill again, and more severely so.

“In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers,” the authors noted. Interestingly, neutralizing antibodies were elicited during this second infection, preventing the animals from being infected a third time. According to the authors:

“Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at risk for severe lung disease on re-exposure to MERS-CoV.”

In other words, if the vaccine does not result in a robust response in neutralizing antibodies, you might be at risk for more severe lung disease if you’re infected with the virus.

And here’s an important point: COVID-19 vaccines are NOT designed to prevent infection. As detailed in “How COVID-19 Vaccine Trials Are Rigged,” a “successful” vaccine merely needs to reduce the severity of the symptoms. They’re not even looking at reducing infection, hospitalization or death rates.

ADE in Dengue Infections

The Dengue virus is also known to cause ADE. As explained in a Swiss Medical Weekly paper published in April 2020:⁸

“The pathogenesis of COVID-19 is currently believed to proceed via both directly cytotoxic and immune-mediated mechanisms. An additional mechanism facilitating viral cell entry and subsequent damage may involve the so-called antibody-dependent enhancement (ADE).

ADE is a very well-known cascade of events whereby viruses may infect susceptible cells via interaction between virions complexed with antibodies or complement components and, respectively, Fc or complement receptors, leading to the amplification of their replication.

This phenomenon is of enormous relevance not only for the understanding of viral pathogenesis, but also for developing antiviral strategies, notably vaccines …

There are four serotypes of Dengue virus, all eliciting protective immunity. However, although homotypic protection is long-lasting, cross-neutralizing antibodies against different serotypes are short-lived and may last only up to 2 years.

In Dengue fever, reinfection with a different serotype runs a more severe course when the protective antibody titer wanes. Here, non-neutralizing antibodies take over neutralizing ones, bind to Dengue virions, and these complexes mediate the infection of phagocytic cells via interaction with the Fc receptor, in a typical ADE.

In other words, heterotypic antibodies at subneutralizing titres account for ADE in persons infected with a serotype of Dengue virus that is different from the first infection.

Cross-reactive neutralizing antibodies are associated with decreased odds of symptomatic secondary infection, and the higher the titer of such antibodies following the primary infection, the longer the delay to symptomatic secondary infection …”

The paper goes on to detail results from follow-up investigations into the Dengue vaccine, which revealed the hospitalization rate for Dengue among vaccinated children under the age of 9 was greater than the rate among controls. The explanation for this appears to be that the vaccine mimicked a primary infection, and as that immunity waned, the children became susceptible to ADE when they encountered the virus a second time. The author explains:

“A post hoc analysis of efficacy trials, using an anti-nonstructural protein 1 immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) to distinguish antibodies elicited by wild-type infection from those following vaccination, showed that the vaccine was able to protect against severe Dengue [in] those who had been exposed to the natural infection before vaccination, and that the risk of severe clinical outcome was increased among seronegative persons.

Based on this, a Strategic Advisor Group of Experts convened by World Health Organization (WHO) concluded that only Dengue seropositive persons should be vaccinated whenever Dengue control programs are planned that include vaccination.”

ADE in Coronavirus Infections

This could end up being important for the COVID-19 vaccine. Hypothetically speaking, if SARS-CoV-2 works like Dengue, which is also caused by an RNA virus, then anyone who has not tested positive for SARS-CoV-2 might actually be at increased risk for severe COVID-19 after vaccination, and only those who have already recovered from a bout of COVID-19 would be protected against severe illness by the vaccine.

To be clear, we do not know whether that is the case or not, but these are important areas of inquiry and the current vaccine trials will simply not be able to answer this important question.

The Swiss Medical Weekly paper⁹ also reviews the evidence of ADE in coronavirus infections, citing research showing inoculating cats against the feline infectious peritonitis virus (FIPV) — a feline coronavirus — increases the severity of the disease when challenged with the same FIPV serotype as that in the vaccine.

The paper also cites research showing “Antibodies elicited by a SARS-CoV vaccine enhanced infection of B cell lines in spite of protective responses in the hamster model.” Another paper,¹⁰ “Antibody-Dependent SARS Coronavirus Infection Is Mediated by Antibodies Against Spike Proteins,” published in 2014, found that:

“… higher concentrations of anti-sera against SARS-CoV neutralized SARS-CoV infection, while highly diluted anti-sera significantly increased SARS-CoV infection and induced higher levels of apoptosis.

Results from infectivity assays indicate that SARS-CoV ADE is primarily mediated by diluted antibodies against envelope spike proteins rather than nucleocapsid proteins. We also generated monoclonal antibodies against SARS-CoV spike proteins and observed that most of them promoted SARS-CoV infection.

Combined, our results suggest that antibodies against SARS-CoV spike proteins may trigger ADE effects. The data raise new questions regarding a potential SARS-CoV vaccine …”

A study¹¹ that ties into this was published in the journal JCI Insight in 2019. Here, macaques vaccinated with a modified vaccinia Ankara (MVA) virus encoding full-length SARS-CoV spike protein ended up with more severe lung pathology when the animals were exposed to the SARS virus. And, when they transferred anti-spike IgG antibodies into unvaccinated macaques, they developed acute diffuse alveolar damage, likely by “skewing the inflammation-resolving response.”

SARS Vaccine Worsens Infection After Challenge With SARS-CoV

An interesting 2012 paper¹² with the telling title, “Immunization with SARS Coronavirus Vaccines Leads to Pulmonary Immunopathology on Challenge with the SARS Virus,” demonstrates what many researchers now fear, namely that COVID-19 vaccines may end up making people more prone to severe SARS-CoV-2 infection.

The paper reviews experiments showing immunization with a variety of SARS vaccines resulted in pulmonary immunophathology once challenged with the SARS virus. As noted by the authors:¹³

“Inactivated whole virus vaccines whether inactivated with formalin or beta propiolactone and whether given with our without alum adjuvant exhibited a Th2-type immunopathologic in lungs after challenge.

As indicated, two reports attributed the immunopathology to presence of the N protein in the vaccine; however, we found the same immunopathologic reaction in animals given S protein vaccine only, although it appeared to be of lesser intensity.

Thus, a Th2-type immunopathologic reaction on challenge of vaccinated animals has occurred in three of four animal models (not in hamsters) including two different inbred mouse strains with four different types of SARS-CoV vaccines with and without alum adjuvant. An inactivated vaccine preparation that does not induce this result in mice, ferrets and nonhuman primates has not been reported.

This combined experience provides concern for trials with SARS-CoV vaccines in humans. Clinical trials with SARS coronavirus vaccines have been conducted and reported to induce antibody responses and to be ‘safe.’ However, the evidence for safety is for a short period of observation.

The concern arising from the present report is for an immunopathologic reaction occurring among vaccinated individuals on exposure to infectious SARS-CoV, the basis for developing a vaccine for SARS. Additional safety concerns relate to effectiveness and safety against antigenic variants of SARS-CoV and for safety of vaccinated persons exposed to other coronaviruses, particularly those of the type 2 group.”

The Elderly Are Most Vulnerable to ADE

On top of all of these concerns, there’s evidence showing the elderly — who are most vulnerable to severe COVID-19 — are also the most vulnerable to ADE. Preliminary research findings¹⁴ posted on the preprint server medRxiv at the end of March 2020 reported that middle-aged and elderly COVID-19 patients have far higher levels of anti-spike antibodies — which, again, increase infectivity — than younger patients.

Immune Enhancement Is a Serious Concern

Another paper worth mentioning is the May 2020 mini review¹⁵ “Impact of Immune Enhancement on COVID-19 Polyclonal Hyperimmune Globulin Therapy and Vaccine Development.” As in many other papers, the authors point out that:¹⁶

“While development of both hyperimmune globulin therapy and vaccine against SARS-CoV-2 are promising, they both pose a common theoretical safety concern. Experimental studies have suggested the possibility of immune-enhanced disease of SARS-CoV and MERS-CoV infections, which may thus similarly occur with SARS-CoV-2 infection …

Immune enhancement of disease can theoretically occur in two ways. Firstly, non-neutralizing or sub-neutralizing levels of antibodies can enhance SARS-CoV-2 infection into target cells.

Secondly, antibodies could enhance inflammation and hence severity of pulmonary disease. An overview of these antibody dependent infection and immunopathology enhancement effects are summarized in Fig. 1 …

Currently, there are multiple SARS-CoV and MERS-CoV vaccine candidates in pre-clinical or early phase clinical trials. Animal studies on these CoVs have shown that the spike (S) protein-based vaccines (specifically the receptor binding domain, RBD) are highly immunogenic and protective against wild-type CoV challenge.

Vaccines that target other parts of the virus, such as the nucleocapsid, without the S protein, have shown no protection against CoV infection and increased lung pathology. However, immunization with some S protein based CoV vaccines have also displayed signs of enhanced lung pathology following challenge.

Hence, besides the choice of antigen target, vaccine efficacy and risk of immunopathology may be dependent on other ancillary factors, including adjuvant formulation, age at vaccination … and route of immunization.”

Do a Risk-Benefit Analysis Before Making Up Your Mind

In all likelihood, regardless of how effective (or ineffective) the COVID-19 vaccines end up being, they’ll be released to the public in relatively short order. Most predict one or more vaccines will be ready sometime in 2021.

Ironically, the data^17,18,19 we now have no longer support a mass vaccination mandate, considering the lethality of COVID-19 is lower than the flu for those under the age of 60.²⁰ If you’re under the age of 40, your risk of dying from COVID-19 is just 0.01%, meaning you have a 99.99% chance of surviving the infection. And you could improve that to 99.999% if you’re metabolically flexible and vitamin D replete.

So, really, what are we protecting against with a COVID-19 vaccine? As mentioned, the vaccines aren’t even designed to prevent infection, only reduce the severity of symptoms. Meanwhile, they could potentially make you sicker once you’re exposed to the virus. That seems like a lot of risk for a truly questionable benefit.

To circle back to where we started, participants in current COVID-19 vaccine trials are not being told of this risk — that by getting the vaccine they may end up with more severe COVID-19 once they’re infected with the virus.

Lethal Th2 Immunopathology Is Another Potential Risk

In closing, consider what this PNAS news feature states about the risk of vaccine-induced immune enhancement and dysfunction, particularly for the elderly, the very people who would need the protection a vaccine might offer the most:²¹

“Since the 1960s, tests of vaccine candidates for diseases such as dengue, respiratory syncytial virus (RSV), and severe acute respiratory syndrome (SARS) have shown a paradoxical phenomenon:

Some animals or people who received the vaccine and were later exposed to the virus developed more severe disease than those who had not been vaccinated. The vaccine-primed immune system, in certain cases, seemed to launch a shoddy response to the natural infection …

This immune backfiring, or so-called immune enhancement, may manifest in different ways such as antibody-dependent enhancement (ADE), a process in which a virus leverages antibodies to aid infection; or cell-based enhancement, a category that includes allergic inflammation caused by Th2 immunopathology. In some cases, the enhancement processes might overlap …

Some researchers argue that although ADE has received the most attention to date, it is less likely than the other immune enhancement pathways to cause a dysregulated response to COVID-19, given what is known about the epidemiology of the virus and its behavior in the human body.

‘There is the potential for ADE, but the bigger problem is probably Th2 immunopathology,’ says Ralph Baric, an epidemiologist and expert in coronaviruses … at the University of North Carolina at Chapel Hill.

In previous studies of SARS, aged mice were found to have particularly high risks of life-threatening Th2 immunopathology ... in which a faulty T cell response triggers allergic inflammation, and poorly functional antibodies that form immune complexes, activating the complement system and potentially damaging the airways.”

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“It seems gene editing is going to eliminate all disease,” said HBO’s John Oliver, “Or kill every last one of us.”¹ He’s referring to gene-editing tools such as CRISPR, or Clustered Regularly Interspaced Short Palindromic Repeat, and TALEN (Transcription Activator-Like Effector Nuclease), which are being used for everything from disease treatment to agriculture.

Unbeknownst to many, CRISPR technology has already been used to tinker with crops, including both plants and animal farming. In addition to altering the taste of foods, CRISPR is being used to extend shelf life and create foods that resist certain bacteria and viruses.²

Even chicken — a staple food in diets around the world — has been eyed for gene editing due to avian leucosis virus, and a “CRISPR” chicken may be coming to your dinner plate soon.

Avian Leukosis Virus Widespread in CAFO Poultry

Avian leukosis virus (ALV) has been plaguing the CAFO (concentrated animal feeding operation) poultry industry since it was first identified in 1991.³ The disease causes tumors to develop in the birds, along with symptoms such as weakness, loss of appetite, diarrhea and depression.⁴

The last major ALV outbreak occurred in 2018 in China, leading to high mortality rates among infected chickens.⁵ However, the virus is present in CAFO chickens worldwide, leading to an estimated millions of pounds of losses annually.⁶

The U.S. Department of Agriculture (USDA) once required that chickens that show signs of ALV or “lesions” (tumors) must be removed from processing so they do not enter the food chain.⁷

However, the National Chicken Council petitioned the USDA’s Food Safety and Inspection Service in March 2019 asking to “treat lesions that could be suspected as being caused by avian leukosis as a trimmable condition and not a condition that requires whole bird condemnation.”⁸

July 16, 2020, FSIS accepted the petition, stating, “We have determined that current scientific evidence supports treating avian leukosis as a trimmable condition and that the actions requested in your petition would reduce regulatory burdens on the industry.”⁹

Despite the significant regulatory change — which means chickens riddled with tumors may still end up in the food supply as long as they’re “trimmed” — researchers have been looking toward gene editing as another way to eradicate ALV from CAFO poultry flocks.

Scientists Use CRISPR to Tackle Avian Leukosis

In 2018, researchers with the Czech Academy of Sciences determined that, because ALVs use specific receptor proteins to gain entry into cells, such receptors would make good targets for “biotechnological manipulation” in order to create poultry resistant to the virus, which they attempted using CRISPR-Cas 9.¹⁰

CRISPR gene-editing technology brought science fiction to life with its ability to cut and paste DNA fragments, potentially eliminating serious inherited diseases. CRISPR-Cas9, in particular, has gotten scientists excited because,¹¹ by modifying an enzyme called Cas9, the gene-editing capabilities are significantly improved.

In their 2018 study, published in the journal Viruses, the scientists noted that “CRISPR/Cas9-mediated knock-out or the fine editing of ALV receptor genes might be the first step in the development of virus-resistant chickens.”¹² In a separate study published in PNAS in January 2020, the researchers demonstrated that CRISPR-Cas9 was effective in rendering chickens resistant to the J subgroup of ALV. They noted:¹³

“We introduced a single amino acid deletion into the gene encoding the receptor that is required for avian leukosis virus subgroup J to infect chicken cells. Here, we demonstrate that this mutation confers the resistance of chickens to avian leukosis virus subgroup J, an important pathogen in poultry. In addition, we present highly efficient genome-editing technology in chicken.”

They added that no visible side effects were apparent after the process, which involved deleting tryptophan residue number 38 of chNHE1 (W38), a critical amino acid for virus entry. The word “visible” is key, however, as many unexpected changes may still occur that aren’t immediately recognizable, and it’s possible for those changes to be transferred to other organisms or generations.

In an interview with Yale Insights, Dr. Greg Licholai, a biotech entrepreneur and a lecturer at Yale, explained that this could even lead to problems that are worse than the “cure,” like antibiotic resistance or incurable diseases:¹⁴

“That’s probably the biggest fear of CRISPR. Humans manipulating the genetic code, and those manipulations get passed on generation to generation to generation.

We think we know what we’re doing, we think we’re measuring exactly what changes we’re doing to the genes, but there’s always the possibility that either we miss something or our technology can’t pick up on other changes that have been made that haven’t been directed by us.

And the fear then is that those changes lead to antibiotic resistance or other mutations that go out into the population and would be very difficult to control. Basically creating incurable diseases or other potential mutations that we wouldn’t really have control over.”

Gene-Edited Chickens Also Exist That Resist Flu

Influenza spreads rapidly among CAFO birds and has the potential to be transmitted to humans. The simplest way to stop the widespread transmission of bird flu would be to change the way chickens are raised, putting them outdoors on pasture as opposed to crowded in disease-ridden CAFOs.

Scientists, however, turned to biotechnology instead, using CRISPR to target part of the ANP32 gene, which codes for a protein that flu viruses depend on,¹⁵ in order to create flu-resistant chickens.¹⁶

Flu- and ALV-resistant chickens are just two examples of gene-editing technology at work. Researchers have also snipped out a section of pig DNA intended to prevent porcine reproductive and respiratory syndrome (PRRS) — a common and often fatal ailment among CAFO pigs.¹⁷ Such edits are permanent and passed down to other generations.

In another project, this one funded by the USDA, researchers have added the SRY gene to cattle, which results in female cows that turn into males, complete with larger muscles, a penis and testicles, but no ability to make sperm.¹⁸ Male (or male-like) cattle are more valuable to the beef industry because they get bigger, faster, allowing companies to make greater profits in less time.

Other biotech companies have taken to targeting genes intended to ease animal suffering, which they believe may soften regulators and consumers who are wary of the technology.¹⁹ One company snipped out the genes responsible for growing horns in dairy cows, for instance, which means they wouldn’t be subjected to the inhumane ways the horns are currently removed (with no pain relief).

As for gene-edited animals, the FDA proposed to classify animals with edited or engineered DNA as drugs,²⁰ prompting backlash from the biotech industry,²¹ which doesn’t even want such foods labeled. This isn’t the case for gene-edited plants, however, which have largely escaped regulation.

Gene-Edited Mushrooms and Lax Regulations

A number of gene-edited plant foods have also been developed or proposed, including non-browning mushrooms, which were created by Yinong Yang, a plant pathologist at Pennsylvania State University, in 2016 using CRISPR-Cas9. Although the “frankenfungi,” as it’s been called, has never before existed in nature, it would require no USDA approval because it does not contain foreign DNA.

"Our genome-edited mushroom has small deletions in a specific gene but contains no foreign DNA integration in its genome," Yang said in Penn State’s Ag Science Magazine. "Therefore, we believed that there was no scientifically valid basis to conclude that the CRISPR-edited mushroom is a regulated article based on the definition described in the regulations."²²

Weeks after the USDA notified Yang that the gene-edited non-browning mushrooms would not require approval, it also ruled that DuPont Pioneer’s CRISPR-Cas9-edited corn would also be able to bypass regulatory approval.²³

The rule, known as the "Sustainable, Ecological, Consistent, Uniform, Responsible, Efficient" (SECURE) rule,²⁴ was finalized in May 2020 and maintained the status that crops edited using CRISPR-Cas9 and other similar technologies would be non-regulated.²⁵

Are You Already Eating Gene-Edited Soybean Oil?

A gene-edited soybean oil created by biotech company Calyxt was picked up by its first user — a Midwest company with both restaurant and foodservice locations, which is using it for frying as well as in dressings and sauces — in 2019.²⁶ Calyxt’s soybean oil, Calyno,²⁷ contains two inactivated genes, resulting in an oil with no trans fats, increased heart-healthy oleic acid and a longer shelf life.

As of February 2019, more than 100 farmers in the Midwest were reportedly growing Calyxt’s high-oleic soybeans on more than 34,000 acres.²⁸ In an update released February 7, 2020, Calyxt stated it had contracted 100,000 soybean acres in the U.S. for 2020, which represented 178% growth from the year prior.²⁹

It also received its first purchase order from a customer targeting four of its primary markets (foodservice, food ingredients, animal nutrition and industrial,) and is now offering 1-gallon jugs of its Calyno cooking oil directly to consumers.³⁰

Calyxt has also developed a high-fiber wheat, which has been declared a non-regulated article and may launch as early as 2020 or 2021.³¹ In short, gene-edited foods are already on the market and expanding with fervor, while the health and environmental risks remain completely unknown.

Unexpected Consequences, Risks Uncovered

Gene-editing, for all of its intended precision, isn’t an exact science. In animals, gene editing has led to unexpected side effects, including enlarged tongues and extra vertebrate.^32,33

Further, when researchers at the U.K.’s Wellcome Sanger Institute systematically studied mutations from CRISPR-Cas9 in mouse and human cells, large genetic rearrangements were observed, including DNA deletions and insertions, near the target site. The DNA deletions could end up activating genes that should stay “off,” such as cancer-causing genes, as well as silencing those that should be “on.”³⁴

Without a label requirement, there’s no way for consumers to know whether they’re eating gene edited soybean oil — or one of the many future gene edited products likely to hit the market, like “CRISPR chicken.” For now, however, gene-edited foods cannot be labeled organic, which is one more reason why seeking out organic and, even better, biodynamic foods, is so important.

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Those following a vegan diet have an increased risk of iodine deficiency.

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Plasma could yield a significant breakthrough in the fight against the spread of COVID-19. In a new study, modeling conducted showed strains of the coronavirus on surfaces like metal, leather, and plastic were killed in as little as 30 seconds of treatment with argon-fed, cold atmospheric plasma.

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Heart attacks strike suddenly and have a range of different triggers. Researchers were able to uncover a further underlying cause. Studying arterial deposits (plaque) in patients with acute coronary syndrome, the researchers found that, in some patients, these were characterized by activated immune cells which, as a result of altered flow conditions within the vessel, had accumulated on the interior arterial wall, causing damage to the arterial lining.

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Those following a vegan diet have an increased risk of iodine deficiency.

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Sensors that monitor a patient's condition during and after medical procedures can be expensive, uncomfortable and even dangerous. Now, an international team of researchers has designed a highly sensitive flexible gas sensor that can be implanted in the body -- and, after it's no longer needed, safely biodegrade into materials that are absorbed by the body.

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New research has cracked a major challenge in the emerging field of nerve engineering. The ink can concentrate neuron growth where it is needed, meticulously guiding cells to regrow in lines between the broken ends of a nerve.

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Microglia -- the brain's immune cells -- play a primary role in removing cellular debris from the brain. A research team has found that another kind of brain cell, called astrocyte, is also involved in removing debris as a backup to microglia.

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Scientists used zebrafish that carry the same genetic mutations as humans with Fragile X syndrome and autism, and discovered the neural networks and pathways that produce the hypersensitivities to sound in both species.

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Being able to feel empathy and to take in the other person's perspective are two abilities through which we understand what is going on in the other's mind. But it is still unclear what exactly they constitute. Researches have now developed a model which explains what empathy and perspective taking are made of: It is not one specific competence rather than many individual factors that vary according to the situation.

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Generating content increases people's enjoyment of positive experiences.

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Severe COVID-19 infection appears rare in newborn babies, suggests a new study. The study traced all babies, less than 29 days old with COVID-19 across the United Kingdom, who needed to be admitted into hospital.

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Measures such as mask wearing and social distancing that are key to reducing coronavirus infection have also greatly reduced the incidence of other diseases, such as influenza and respiratory syncytial virus (RSV). But researchers report that current reductions in these common respiratory infections, however, may increase people's susceptibility to these diseases, resulting in large future outbreaks when they begin circulating again.

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A new study shows flame retardants found in nearly every American home cause mice to give birth to offspring that become diabetic.

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N-acetylcysteine (NAC) is a precursor to reduced glutathione, which appears to play a crucial role in COVID-19. According to an April 2020 literature analysis,¹ glutathione deficiency may be associated with COVID-19 severity, leading the author to conclude that NAC may be useful both for its prevention and treatment.

NAC has a long history of use as a first-aid remedy for acetaminophen poisoning. It neutralizes the toxic effects of the drug by recharging glutathione, thereby preventing liver damage. But the idea that NAC can also be helpful against viral infections is not new. Previous studies^2,3 have found it reduces viral replication of certain viruses, including the influenza virus.

In one such study,⁴ the number needed to treat (NNT) was 0.5, which means for every two people treated with NAC, one will be protected against symptomatic influenza. That’s significantly better than influenza vaccines, which have an NNV (number needed to vaccinate) of 71,⁵ meaning 71 people must be vaccinated to prevent a single case of confirmed influenza. It’s even better than vitamin D, which has an NNT of 33.⁶

In the MedCram lecture above, pulmonologist Dr. Roger Seheult reviews the latest medical literature on NAC for COVID-19, starting with a paper⁷ published in the October 2020 issue of Clinical Immunology titled “Therapeutic Blockade of Inflammation in Severe COVID-19 Infection With Intravenous N-acetylcysteine.”

G6PD Deficiency Worsens COVID-19 Outcomes

Previous research⁸ has shown NAC inhibits the expression of proinflammatory cytokines in cells infected with highly pathogenic H5N1 influenza virus. Proinflammatory cytokines also play a crucial role in COVID-19 severity.

Researchers have confirmed that in severe COVID-19 cases, cytokines such as interleukin-6 (IL6), interleukin-10 (IL10) and TNF-ɑ are all elevated.⁹ Once they reach excessive levels, a so-called cytokine storm develops, causing significant tissue damage. NAC may be able to inhibit this damaging cascade.

In the “Therapeutic Blockade of Inflammation in Severe COVID-19 Infection With Intravenous N-acetylcysteine” paper, the researchers focus on a specific group of patients, namely those with glucose 6-phosphate dehydrogenase (G6PD) deficiency, which has been shown to facilitate human coronavirus infection due to the fact that G6PD depletes glutathione. 

G6PD deficiency¹⁰ is a genetic disorder that typically affects males and is more prevalent among Black men and those from the Mediterranean area, Africa and Asia. (Women with this genetic anomaly are carriers and can pass it on to their children but rarely display symptoms.)

G6PD is an enzyme needed for the proper function of red blood cells. It also protects your red blood cells from free radicals in your blood by limiting oxidative stress.

When your body doesn’t produce enough of this enzyme, hemolytic anemia — a condition in which red blood cells are broken down faster than they are made — can result due to unneutralized oxidative stress from insufficient amounts of NADPH being produced.

As noted in “Therapeutic Blockade of Inflammation in Severe COVID-19 Infection With Intravenous N-acetylcysteine”:¹¹

“G6PD deficiency may especially predispose to hemolysis upon coronavirus disease-2019 (COVID-19) infection when employing pro-oxidant therapy. However, glutathione depletion is reversible by N-acetylcysteine (NAC) administration.

We describe a severe case of COVID-19 infection in a G6PD-deficient patient treated with hydroxychloroquine who benefited from intravenous (IV) NAC beyond reversal of hemolysis.

NAC blocked hemolysis and elevation of liver enzymes, C-reactive protein (CRP), and ferritin and allowed removal from respirator and veno-venous extracorporeal membrane oxygenator and full recovery of the G6PD-deficient patient.”

How G6PD Deficiency Impacts COVID-19 Disease Process

In his lecture, Seheult goes through the nitty-gritty details of how G6PD influences the COVID-19 disease process, why a deficiency in this enzyme can worsen outcomes and how NAC supplementation short-circuits this harmful chain of events.

In summary, hydrogen peroxide (H₂O₂), a reactive oxygen species (ROS), needs to be converted to water (H₂O) as much as possible in your cells to avoid red blood cell hemolysis, i.e., the destruction of red blood cells.

As noted by Seheult, there’s concern that the drug hydroxychloroquine may increase this process in G6PD-deficient patients, thereby increasing the risk of red blood cell hemolysis.¹²

The evidence is not conclusive, however. One 2018 study¹³ looking at the incidence of hemolytic anemia in G6PD-deficient patients given hydroxychloroquine concluded the risk may be overblown, as “There were no reported episodes of hemolysis in more than 700 months of HCQ exposure among the 11 G6PDH-deficient patients.”

The enzyme responsible for the conversion of hydrogen peroxide to water is glutathione peroxidase (GPX). GPX does two things simultaneously. While reducing hydrogen peroxide into water, it also converts the reduced form of glutathione (GSH) into glutathione disulfide (GSSG), which is the oxidized form of glutathione. In other words, as GPX turns hydrogen peroxide into harmless water, glutathione becomes oxidized.

To recycle GSSG back to its reduced form, GSH, you need an enzyme called GSH reductase. The reducing agent needed for this to occur is NADPH. NADPH is also simultaneously converted into NADP+. To recycle NADP+ back to NADPH, you need G6PD.

The point here is this: Patients who have G6PD deficiency will also have lower NADPH, and therefore won’t be able to reduce the GSSG (the oxidated form of glutathione) to its reduced GSH form. This in turn leads to a buildup of hydrogen peroxide, resulting in higher levels of hemolysis.

As explained by Seheult, the two building blocks of glutathione are NAC and the amino acid glycine. Glycine is fairly abundant, whereas NAC is not, so the theory is that, if you are G6PD deficient, you may be able to bypass this detrimental spiral by supplying high levels of NAC. This will allow your body to produce its own glutathione (GSH).

This theory is what was investigated in “Therapeutic Blockade of Inflammation in Severe COVID-19 Infection With Intravenous N-acetylcysteine,”¹⁴ and the answer is yes. When given hydroxychloroquine, the G6PD-deficient patient developed severe hemolysis, which was successfully reversed by giving intravenous NAC. In the end, the patient fully recovered.

As for the dosage, the G6PD-deficient patient was given 30,000 milligrams of intravenous NAC divided into three doses over 24 hours, after which the patient began showing immediate improvement in hemolysis indices. About a week later, IV NAC was restarted at a dose of 600 mg every 12 hours for one week.

NAC Blocks Inflammation

In addition to that G6PD-deficient patient, NAC was also given to nine other COVID-19 patients who were on respirators but did not have G6PD deficiency. In these patients, “NAC elicited clinical improvement and markedly reduced CRP in all patients and ferritin in 9/10 patients.” The authors hypothesize that NAC’s mechanism of action “may involve the blockade of viral infection and the ensuing cytokine storm.”¹⁵

That said, they point out that it’s difficult to discern whether these anti-inflammatory effects were specific to the use of NAC, as steroids and other anti-inflammatory drugs were sporadically used. Still, they believe NAC does have the ability to reduce inflammation in patients with COVID-19. As explained in the paper:¹⁶

“We propose that NAC restrains the pro-inflammatory metabolic pathways that control oxidative stress and mTOR-dependent generation of cytokine storm emanating from the immune system …

IL-6, the primary cytokine that drives inflammation in COVID-19 infected patients, elicits mitochondrial oxidative stress at complex I of the mitochondrial electron transport chain (ETC). In turn, this leads to redox-dependent activation of mTORC1.

Further downstream, uncontrolled activation of mTORC1 promotes inflammation. NAC inhibits oxidative stress by serving as a cell-permeable amino acid precursor of the main intracellular antioxidant, GSH.

Acting outside the cell, NAC may break disulfide bonds within ACE2 that serves as the cellular receptor for COVID-19. NAC may also block COVID-19 binding by disrupting disulfide bind within its receptor-binding domain …

Several anti-inflammatory medications have been shown to mitigate the cytokine storm in COVID-19 infection, such as corticosteroids, colchicine, imatinib, and complement C3 inhibitor AMY-101. However, the safety of mTOR blockade stands out based on its propensity to extend overall lifespan.

IV NAC has long been used to safely treat patients with acetaminophen overdose, or ARDS [acute respiratory distress syndrome]. NAC was also found to reduce CRP levels in several controlled clinical trials. CRP elevation is a prominent risk factor for disease progression in patients infected with COVID-19.”

NAC Also Protects Against Blood Clots

Importantly, NAC may also protect against other problems associated with COVID-19, including the hypercoagulation that can result in stroke and/or blood clots¹⁷ that impair the ability to exchange oxygen in the lungs.

Many COVID-19 patients experience serious blood clots, and NAC counteracts hypercoagulation,^18,19,20 as it has both anticoagulant and platelet-inhibiting properties.²¹ A 2017 paper²² also found NAC has potent thrombolytic effects, meaning it breaks down blood clots once they’ve formed.

This is largely thanks to the sulfur in NAC (from cysteine). The sulfur reduces the intrachain disulfide bonds by von Willebrand factors that have polymerized by dissociating the sulfur bonds holding them together, thus contributing to the clot. Once von Willebrand factor sulfur bonds are broken, the clots start to dissolve and the blood vessels open up again allowing for exchange of oxygen and carbon dioxide.

According to the authors,²³ “NAC is an effective and safe alternative to currently available antithrombotic agents to restore vessel patency after arterial occlusion.” (Restoring vessel patency means the blood vessel is now unobstructed so that blood can flow freely.) Two additional papers^24,25 show the same thing.

Importantly, NAC’s mechanism of action does not appear to increase bleeding disorders like heparin does, so it would likely be a safer alternative to the heparin used in the MATH+ protocol.

NAC Also Improves Variety of Lung-Related Problems

Studies have also demonstrated that NAC helps improve a variety of lung-related problems, including pneumonia and ARDS,²⁶ both of which are common characteristics of COVID-19. For example:

Research27 published in 2018 found NAC reduces oxidative and inflammatory damage in patients with community-acquired pneumonia.

Another 2018 study28 found NAC improves post-operative lung function in patients undergoing liver transplantation.

A 2017 meta-analysis29 found a significant reduction in ICU stays among ARDS patients treated with NAC (although there was no significant difference in short-term mortality risk).

A 2007 study30 concluded NAC improves ARDS by “increasing intracellular glutathione and extracellular thiol molecules” along with general antioxidant effects.

A 1994 study31 found NAC enhances recovery from acute lung injury, significantly regressing patients’ lung injury score during the first 10 days of treatment, and significantly reducing the need for ventilation. After three days of treatment, only 17% of those receiving NAC needed ventilation, compared to 48% in the placebo group.

NAC is also a well-known mucolytic used to help clear mucus out of the airways of cystic fibrosis patients.32 Some studies also suggest NAC can help reduce symptoms of COPD and prevent exacerbation of the condition.33

Standard of Care for COVID-19 Should Include NAC

Considering many COVID-19 cases involve blood clots in addition to excessive oxidative stress, and NAC effectively addresses both, I believe NAC should be included in standard of care for COVID-19. As noted in “Rationale for the Use of N-acetylcysteine in Both Prevention and Adjuvant Therapy of COVID-19,” published August 11, 2020, in the FASEB Journal:³⁴

“COVID-19 may cause pneumonia, acute respiratory distress syndrome, cardiovascular alterations, and multiple organ failure, which have been ascribed to a cytokine storm, a systemic inflammatory response, and an attack by the immune system. Moreover, an oxidative stress imbalance has been demonstrated to occur in COVID-19 patients.

N- Acetyl-L-cysteine (NAC) is a precursor of reduced glutathione (GSH). Due to its tolerability, this pleiotropic drug has been proposed not only as a mucolytic agent, but also as a preventive/therapeutic agent in a variety of disorders involving GSH depletion and oxidative stress …

Thiols block the angiotensin-converting enzyme 2 thereby hampering penetration of SARS-CoV-2 into cells. Based on a broad range of antioxidant and anti-inflammatory mechanisms … the oral administration of NAC is likely to attenuate the risk of developing COVID-19, as it was previously demonstrated for influenza and influenza-like illnesses.

Moreover, high-dose intravenous NAC may be expected to play an adjuvant role in the treatment of severe COVID-19 cases and in the control of its lethal complications … including pulmonary and cardiovascular adverse events.”

In the same vein, an even more recent paper,³⁵ published in the October 2020 issue of Medical Hypotheses, points out that:

“T cell exhaustion, high viral load, and high levels of TNF-ɑ, IL1β, IL6, IL10 have been associated with severe SARS-CoV-2. Cytokine and antigen overstimulation are potentially responsible for poor humoral response to the virus. Lower cellular redox status, which leads to pro-inflammatory states mediated by TNF-ɑ is also potentially implicated. 

In vivo, in vitro, and human clinical trials have demonstrated N-acetylcysteine (NAC) as an effective method of improving redox status, especially when under oxidative stress.

In human clinical trials, NAC has been used to replenish glutathione stores and increase the proliferative response of T cells. NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1β and IL18) in vitro, and decrease plasma TNF-ɑ in human clinical trials.

Mediation of the viral load could occur through NAC’s ability to increase cellular redox status via maximizing the rate limiting step of glutathione synthesis, and thereby potentially decreasing the effects of virally induced oxidative stress and cell death.

We hypothesize that NAC could act as a potential therapeutic agent in the treatment of COVID-19 through a variety of potential mechanisms, including increasing glutathione, improving T cell response, and modulating inflammation.”

FDA Cracks Down on NAC and Wants to Prevent You From Using It

At present, 11 studies involving NAC for COVID-19 are listed on Clinicaltrials.gov.³⁶ Ironically, just as we’re starting to realize its benefits against this pandemic virus, the U.S. Food and Drug Administration is suddenly cracking down on NAC, claiming it is excluded from the definition of a dietary supplement.

They point out that NAC was approved as a new drug in 1985,³⁷ and therefore cannot be marketed as a supplement. This is not reflected in the supplement market, however. As reported by Natural Products Insider,³⁸ there are at least 1,170 NAC-containing products in the National Institutes of Health’s Dietary Supplement Label Database.

As of yet, the FDA has not taken action against NAC due to anything related to COVID-19. They’ve primarily targeted companies that market NAC as a remedy for hangovers.³⁹ Still, members of the Council for Responsible Nutrition have expressed concern the FDA may end up targeting NAC more widely. Hopefully, the FDA will not end up blocking access to NAC supplements in the same way hydroxychloroquine access has been stifled.

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Up to half a million barrels of toxic DDT (dichloro-diphenyl-trichloroethane) waste may be sitting discarded on the ocean floor, off the coast of Los Angeles, California.

In a chilling exposé by Rosanna Xia, an environment reporter for the Los Angeles Times, photos taken by a deep-sea robot show barrels covered in sediment, some with slashes through them because, “when the barrels were too buoyant to sink on their own, one report said, the crews simply punctured them.”¹

Some of the other more disturbing elements uncovered were shipping logs that show thousands of barrels of DDT-laced acid sludge were dumped into the ocean each month following World War II.

And while workers were supposed to go out to “Dumpsite No. 1,” located about 10 nautical miles northwest of Catalina Island, “Regulators reported in the 1980s that the men in charge of getting rid of the DDT waste sometimes took shortcuts and just dumped it closer to shore.”² Rumblings of a secret dumpsite in the deep ocean have been going on for decades, but only a handful of individuals have followed the story.

What they’ve uncovered suggests the toxic dumping ground could be slowly releasing poison into the ocean environment or, perhaps worse, could one day explode copious amounts into the surrounding area, contaminating it with DDT at unprecedented levels. Perhaps even more unsettling, no one seems to know what to do about it.

California Was Home to the Largest DDT Producer

Montrose Chemical Corp. opened a plant near Torrance, California, in 1947 to manufacture DDT. It was the largest such manufacturer in the U.S., operating from 1947 to 1982. To this day, the plant’s site is regarded as one of the most hazardous in the U.S., but at the time DDT was thought of as a wonder chemical.

“The chemical industry was celebrated at the time for boosting the nation into greater prosperity and preventing crop failures across the globe. The United States used as much as 80 million pounds of DDT in one year,” Xia wrote, above a photo showing beachgoers frolicking in massive DDT clouds, which were sprayed on U.S. beaches to eliminate mosquitoes.

It would be nearly two decades before marine biologist Rachel Carson would sound the alarm that chemicals like DDT were destroying nature. In the meantime, DDT was praised as “the war’s greatest contribution to the future health of the world” by Brig. Gen. James Simmons, the U.S. Army’s chief of preventive medicine, during World War II — a time when the chemical was sprayed onto soldiers to protect them from malaria and typhus.³

Montrose quickly became a key player in supplying governments around the globe with DDT, and even continued to produce it for another 10 years after it was banned in the U.S. in 1972. “Demand was still strong in other countries,” Xia noted, “… so the chemical plant in Los Angeles kept churning out more.”⁴

In its early years of production, the ocean was considered to be an acceptable place to dispose of waste. “Dilution is the solution to pollution, the saying used to go,” the article quips, but with chemicals as toxic as DDT, there’s only so much the environment can take.

In addition to being very persistent in the environment, DDT is known to accumulate in fatty tissues and travels long distances in the upper atmosphere.⁵ It’s because of its persistence in the environment that even residues (or barrels of them) dumped decades ago remain a significant environmental and human health concern.

Underwater Robot Reveals Toxic DDT Legacy

David Valentine, a professor of geochemistry and microbiology at UC Santa Barbara, and Veronika Kivenson, a Ph.D. student in marine science, were among a team of scientists who published research showing that the ocean dumping of DDT waste was a “sloppy process,” and the barrels on the ocean floor are “readily breaching containment and leading to regional scale contamination of the deep benthos.”⁶

They cited a technical report by Allan Chartrand, a former scientist at the California Regional Water Quality Control Board in Los Angeles, who estimated the area may contain 336,000 to 504,000 barrels of acid sludge waste contaminated with residues of DDT.

The barrels were dumped by Montrose at an estimated rate of 2,000 to 3,000 per month — an amount equal to about 1 million gallons of waste per year — from 1947 to 1961.⁷ This was a legal process at the time, and the researchers suggested the waste may contain 0.5% to 2% DDT, amounting to a total DDT discharge of 384 tons to 1,535 tons.⁸ As Xia wrote:⁹

“Federal ocean dumping laws dated back to 1886, but the rules were focused on clearing the way for ship navigation. It wasn’t until the Marine Protection, Research and Sanctuaries Act of 1972, also known as the Ocean Dumping Act, that environmental impacts were considered. Dumping industrial chemicals near Catalina was an accepted practice for decades.”

Montrose Already Involved in Toxic Superfund Site

This wasn’t Montrose’s only offense, however. The company also discharged DDT-laden waste into storm drains and sewer systems from 1950 to 1971. This contaminated the Palos Verdes Shelf with up to 1,450 tons of DDT, the ramifications of which are still being dealt with today.

After being declared a 17-square mile Superfund site in 1996, a more than $140 million settlement agreement was reached, to be paid by Montrose, local governments and several other companies connected to the plant.

“The settlement — one of the largest in the nation for an environmental damage claim — would pay for cleanup, habitat restoration and education programs for people at risk of eating contaminated fish,” according to Xia, but after decades of studies and meetings trying to determine how to clean up the site, efforts have stalled, and an EPA review suggests DDT levels have been slowly declining anyway.¹⁰

“To have the EPA say, 25 years later, that maybe the best thing to do is to just let nature take its course is, frankly, nothing short of nauseating,” Mark Gold, a marine scientist who’s worked closely with the DDT issue, told Xia.¹¹

In August 2020, Montrose reached another settlement agreement, this time for $56.6 million, over groundwater contamination, but neither of the prior settlements address the potential devastation that could be caused by the deep-sea dumping site. Samples of sediment in the area revealed DDT concentrations up to 40 times higher than the greatest concentration found at the Palos Verdes Superfund site.¹²

DDT’s Toxic Effects

Exposure to DDT is linked to reproductive effects in humans, and the chemical is classified as a probable human carcinogen that’s been linked to liver tumors in animal studies.¹³ Like many environmental toxins, DDT passes freely through the placenta during pregnancy, where it gains direct access to the developing fetus and may have lifelong ramifications.

One study revealed that women exposed to the most DDT before birth were 2.5 to 3.6 times more likely to develop high blood pressure before the age of 50 than those with the lowest prenatal exposure.¹⁴

Elevated levels of DDT are also associated with high blood pressure in adults,¹⁵ while exposure to DDT is also known to induce epigenetic changes that promote obesity and kidney, testis and ovary disease that are passed on to future generations.¹⁶ Other toxic effects of DDT exposure in humans include:¹⁷

• Developmental abnormalities
• Reproductive disease
• Neurological disease
• Cancer

Environmentally, significant harms have also been exposed by various people and publications, beginning with Carson’s book “Silent Spring” more than five decades ago. Biologists learned that pesticides like DDT were bio-accumulating in wildlife and becoming more concentrated as they moved up the food chain. Birth defects in wildlife have also been linked to the chemical,¹⁸ which is linked to a wide range of negative environmental impacts.

Among them, pelican eggshells with the highest concentrations of DDT were thinner than those with the lowest concentrations, which suggests exposure poses a risk of reproductive impairment.¹⁹

It was also due to DDT that bald eagle populations were decimated in the U.S. After contaminating waterways and fish — one of eagles’ favorite foods — eagles were poisoned by DDT and produced eggs with thin shells that often broke before their offspring could hatch.²⁰

While DDT is now banned in the U.S., it’s still used in certain countries as a pesticide to control mosquitoes that may transmit malaria. The Stockholm Convention in 2001 called on countries to eliminate their use of DDT, but, as reported in Environmental Health, “Due to the … Gates Foundation Malaria Control Program the use of DDT in Africa and other parts of the world has increased.”²¹

‘We Still Don’t Have a Plan’

While it’s clear that DDT is one of the most widespread pollutants of our time, what to do about it remains much more of a mystery. As usage continues in some parts of the world, researchers wrote in Chemosphere:²²

“Our findings suggest continued negative human health and environmental impacts from DDT. There is an urgency to move away from DDT as quickly as possible; alternatively, to implement practices that prevent emissions of DDT to the environment while protecting human life.”

The far-reaching health effects continue to be uncovered. In 2016, it was revealed that DDT may inhibit P-glycoprotein, a “defense protein” that’s important for protecting organisms against environmental toxins.²³ “Even in small amounts, these contaminants could interfere with the human body’s natural ability to defend itself,” Xia noted.²⁴

Meanwhile, hundreds of thousands of DDT-contaminated waste barrels are sitting on the ocean floor, likely sending a steady stream of the poison into the open ocean. When researchers tested the blubber of eight southern California bottlenose dolphins, it contained 45 bioaccumulative DDT-related compounds, 80% of which are not typically monitored.²⁵

The dolphins lived in deeper waters, which was why researchers were surprised at their results, which showed higher levels of DDT than dolphins tested in Brazil and other areas. As for the DDT dumping ground, “These barrels do seem to be leaking over time,” Kivenson told Xia. “This toxic waste is just kind of bubbling down there, seeping, oozing, I don’t know what word I want to use … It’s not a contained environment.”²⁶

Unfortunately, as is the case with many environmental pollutants, the cleanup process is complex, even insurmountable. Once the problem is detected, as is now becoming evident off the California coast, the next question is what to do about it. “These chemicals are still out there, and we haven’t figured out what to do,” Amro Hamdoun with the Scripps Institution of Oceanography told Xia. “They are an issue, and we still don’t have a plan.”²⁷

Adding to the problem, even though DDT was banned in the U.S., it was simply replaced with other equally unsafe and untested chemicals, such as glyphosate, adding multiple layers of chemical exposures to an already adulterated environment. Your best option now and in the future is to take steps to avoid environmental pollutants as much as possible while adding in elements to help your body detoxify.

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