Scientist admits the ‘overwhelming consensus’ on the climate change crisis is ‘manufactured’

 We are told climate change is a crisis, and that there is an “overwhelming scientific consensus.”

“It’s a manufactured consensus,” climate scientist Judith Curry tells me.

She says scientists have an incentive to exaggerate risk to pursue “fame and fortune.”

She knows about that because she once spread alarm about climate change.

Media loved her when she published a study that seemed to show a dramatic increase in hurricane intensity.

“We found that the percent of Category 4 and 5 hurricanes had doubled,” says Curry.

“This was picked up by the media,” and then climate alarmists realized, “Oh, here is the way to do it. Tie extreme weather events to global warming!”

“So, this hysteria is your fault!” I tell her.

“Not really,” she smiles.

“They would have picked up on it anyways.”

Curry claims scientists have an incentive to exaggerate risk to pursue “fame and fortune” regarding to climate change.

REUTERS

But Curry’s “more intense” hurricanes gave them fuel.

“I was adopted by the environmental advocacy groups and the alarmists and I was treated like a rock star,” Curry recounts.

“Flown all over the place to meet with politicians.”

But then some researchers pointed out gaps in her research — years with low levels of hurricanes.

“Like a good scientist, I investigated,” says Curry.

Curry adds on, “This was picked up by the media,” and then climate alarmists realized, “Oh, here is the way to do it. Tie extreme weather events to global warming!”

ZUMAPRESS.com

She realized that the critics were right.

“Part of it was bad data. Part of it is natural climate variability.”

Curry was the unusual researcher who looked at criticism of her work and actually concluded “they had a point.”

Then the Climategate scandal taught her that other climate researchers weren’t so open-minded.

Alarmist scientists’ aggressive attempts to hide data suggesting climate change is not a crisis were revealed in leaked emails.

In regards to the Climategate scandal, it taught Curry that other climate researchers weren’t so open-minded.

AFP via Getty Images

“Ugly things,” says Curry.

“Avoiding Freedom of Information Act requests. Trying to get journal editors fired.”

It made Curry realize that there is a “climate-change industry” set up to reward alarmism.

“The origins go back to the . . . UN environmental program,” says Curry.

Some United Nations officials were motivated by “anti-capitalism. They hated the oil companies and seized on the climate change issue to move their policies along.”

The UN created the Intergovernmental Panel on Climate Change.

“The IPCC wasn’t supposed to focus on any benefits of warming. The IPCC’s mandate was to look for dangerous human-caused climate change.”

“Then the national funding agencies directed all the funding . . . assuming there are dangerous impacts.”

The researchers quickly figured out that the way to get funded was to make alarmist claims about “man-made climate change.”

This is how “manufactured consensus” happens.

Even if a skeptic did get funding, it’s harder to publish because journal editors are alarmists.

“The editor of the journal Science wrote this political rant,” says Curry.

She even said, “The time for debate has ended.”

“What kind of message does that give?” adds Curry.

Then she answers her own question: “Promote the alarming papers! Don’t even send the other ones out for review. If you wanted to advance in your career, like be at a prestigious university and get a big salary, have big laboratory space, get lots of grant funding, be director of an institute, there was clearly one path to go.” 

That’s what we’ve got now: a massive government-funded climate alarmism complex.

John Stossel is the author of “Give Me a Break: How I Exposed Hucksters, Cheats, and Scam Artists and Became the Scourge of the Liberal Media.”

https://nypost.com/2023/08/09/climate-scientist-admits-the-overwhelming-consensus-is-manufactured/

Long-term use of certain acid reflux drugs linked to higher risk of dementia

 People who take acid reflux medications called proton pump inhibitors for four-and-a-half years or more may have a higher risk of dementia compared to people who do not take these medications, according to new research published in Neurology. This study does not prove that acid reflux drugs cause dementia; it only shows an association.

Acid reflux is when stomach acid flows into the esophagus, usually after a meal or when lying down. People with acid reflux may experience heartburn and ulcers. People with frequent acid reflux may develop gastroesophageal reflux disease, or GERD, which can lead to cancer of the esophagus.

Proton pump inhibitors reduce stomach acid by targeting the enzymes in the stomach lining that produce that acid.

"Proton pump inhibitors are a useful tool to help control acid reflux, however long-term use has been linked in previous studies to a higher risk of stroke, bone fractures and chronic kidney disease," said study author Kamakshi Lakshminarayan, MBBS, Ph.D., of the University of Minnesota School of Public Health in Minneapolis, and a member of the American Academy of Neurology.

"Still, some people take these drugs regularly, so we examined if they are linked to a higher risk of dementia. While we did not find a link with short-term use, we did find a higher risk of dementia associated with long-term use of these drugs."

The study included 5,712 people, age 45 and older, who did not have dementia at the start of the study. They had an average age of 75.

Researchers determined if participants took acid reflux drugs by reviewing their medications during study visits and during yearly phone calls. Of the participants, 1,490 people, or 26%, had taken the drugs. Participants were then divided into four groups based on whether they had taken the drugs and for how long, as follows: people who did not take the drugs; those who took the drugs for up to 2.8 years; those who took them for 2.8 to 4.4 years; and people who took them for more than 4.4 years.

Participants were then followed for a median duration of 5.5 years. During this time, 585 people, or 10%, developed dementia.

Of the 4,222 people who did not take the drugs, 415 people developed dementia, or 19 cases per 1,000 person-years. Person-years represent both the number of people in the study and the amount of time each person spends in the study. Of the 497 people who took the drugs for more than 4.4 years, 58 people developed dementia, or 24 cases per 1,000 person years.

After adjusting for factors such as age, sex and race, as well as health-related factors such as high blood pressure and diabetes, researchers found people who had been taking acid reflux drugs for more than 4.4 years had a 33% higher risk of developing dementia than people who never took the drugs.

Researchers did not find a higher risk of dementia for people who took the drugs for fewer than 4.4 years.

"More research is needed to confirm our findings and explore reasons for the possible link between long-term proton pump inhibitor use and a higher risk of dementia," said Lakshminarayan.

"While there are various ways to treat acid reflux, such as taking antacids, maintaining a healthy weight, and avoiding late meals and certain foods, different approaches may not work for everyone. It is important that people taking these medications speak with their doctor before making any changes, to discuss the best treatment for them, and because stopping these drugs abruptly may result in worse symptoms."

A limitation of the study was that participants were asked once a year about medication use, so researchers estimated use between annual check-ins. If participants stopped and restarted acid reflux drugs in between check-ins, estimation of their use may have been inaccurate. The authors were also unable to assess if participants took over the counter acid reflux drugs.

More information: Kamakshi Lakshminarayan et al, Neurology (2023).

https://medicalxpress.com/news/2023-08-long-term-acid-reflux-drugs-linked.html#google_vignette

Stem cell therapy rescues symptoms of Alzheimer's disease

 In the ongoing search for a cure for Alzheimer's disease, a burgeoning branch of medicine is bringing new hope. Stem cell therapies are already being used to treat various cancers and disorders of the blood and immune system. In a new proof-of-concept study, scientists at University of California San Diego show stem cell transplants may also be a promising therapeutic against Alzheimer's.

In the study, publishing this month in Cell Reports, the researchers demonstrate that transplanting hematopoietic stem and progenitor cells was effective in rescuing multiple signs and symptoms of Alzheimer's in a mouse model of the disease. Mice that received healthy hematopoietic stem cells showed preserved memory and cognition, reduced neuroinflammation and significantly less β-amyloid build-up compared to other Alzheimer's mice.

"Alzheimer's is a very complex disease, so any potential treatment has to be able to target multiple biological pathways," said senior study author Stephanie Cherqui, Ph.D., professor at UC San Diego School of Medicine. "Our work shows that hematopoietic stem and progenitor cell transplantation has the potential to prevent complications from Alzheimer's and could be a promising therapeutic avenue for this disease."

The success of the therapy stems from its effects on microglia, a type of immune cell in the brain. Microglia have been implicated in the initiation and progression of Alzheimer's disease in various ways. It's known that sustained microglia inflammation can contribute to Alzheimer's, as the release of inflammatory cytokines, chemokines and complement proteins leads to increased β-amyloid production. In healthy conditions, microglia also play a major role in clearing β-amyloid plaques, but this function is impaired in Alzheimer's. The resulting β-amyloid build-up also puts stress on other brain cells, including endothelial cells that affect blood flow to the brain.

Postdoctoral researcher and first author Priyanka Mishra, Ph.D., set out to test whether transplanting stem cells could lead to the generation of new, healthy microglia that might reduce the progression of Alzheimer's disease. The Cherqui lab had already found success using similar stem cell transplants to treat mouse models of cystinosis, a lysosomal storage disease, and Friedreich's ataxia, a neurodegenerative disease.

Mishra and her colleagues performed systemic transplantations of healthy wild-type hematopoietic stem and progenitor cells into Alzheimer's mice and found that the transplanted cells did differentiate into microglia-like cells in the brain.

The researchers then evaluated the animals' behavior and found that memory loss and neurocognitive impairment were completely prevented in mice that received the stem cell transplant. These mice showed better object recognition and risk perception, as well as normal anxiety levels and locomotor activity, compared to non-treated Alzheimer's mice.

Looking closer at the animals' brains, the researchers found that mice treated with healthy stem cells showed a significant reduction in β-amyloid plaques in their hippocampus and cortex. The transplant also led to reduced microgliosis and neuroinflammation, and helped preserve the integrity of the blood-brain barrier.

Finally, the researchers used transcriptomic analyses to measure the expression of different genes in treated and non-treated Alzheimer's mice. Those that had received the stem cell therapy had less cortical expression of genes associated with diseased microglia, and less hippocampal expression of genes associated with diseased endothelial cells.

Altogether, the transplantation of healthy hematopoietic stem and progenitor cells led to enhanced microglia health, which in turn protected against multiple levels of Alzheimer's pathology.

Importantly, a third group of mice that received stem cells isolated from Alzheimer's mice exhibited no signs of improvement, demonstrating that these cells retained the disease-related information in Alzheimer's disease.

Future studies will further explore how the healthy transplanted cells produced such significant improvements, and whether similar transplant strategies can be used to alleviate Alzheimer's symptoms in humans.

"Alzheimer's disease poses a major emotional and economic burden on our society, yet there is no effective treatment available," said Cherqui. "We are excited to see such promising preclinical results from hematopoietic stem cell therapy and look forward to developing a new therapeutic approach for this devastating disease."

Co-authors of the study include: Alexander Silva, Jay Sharma, Jacqueline Nguyen, Donald P. Pizzo and Debashis Sahoo, all at UC San Diego, as well as Denise Hinz at the La Jolla Institute for Immunology.

More information: Priyanka Mishra et al, Rescue of Alzheimer's disease phenotype in a mouse model by transplantation of wild-type hematopoietic stem and progenitor cells, Cell Reports (2023). DOI: 10.1016/j.celrep.2023.112956

https://medicalxpress.com/news/2023-08-stem-cell-therapy-symptoms-alzheimer.html

Synthetic antibiotic could be effective against drug-resistant superbugs

 A scientific journey decades in the making at Duke University has found a new antibiotic strategy to defeat gram-negative bacteria like Salmonella, Pseudomonas and E. coli, the culprits in many urinary tract infections (UTIs). The synthetic molecule works fast and is durable in animal tests.

It works by interfering with a bacterium's ability to make its outer lipid layer. "If you disrupt the synthesis of the bacterial outer membrane, the bacteria cannot survive without it," said lead investigator Pei Zhou, a professor of biochemistry in the Duke School of Medicine. "Our compound is very good and very potent."

The compound, called LPC-233, is a small molecule that has proven effective at wrecking the outer membrane lipid biosynthesis in every gram-negative bacterium it was tested against. Co-authors at the University of Lille in France tested it against a collection of 285 bacterial strains, including some that were highly resistant to commercial antibiotics, and it killed them all.

And it works fast. "LPC-233 can reduce bacterial viability by 100,000-fold within four hours," Zhou said.

The compound is also tenacious enough to survive all the way to the urinary tract after oral administration, which may make it a vital tool against stubborn urinary tract infections (UTIs).

Tests run at high concentrations of the compound showed "exceedingly low rates of spontaneous resistance mutations in these bacteria," according to a paper describing the findings, which appears in Science Translational Medicine.

In animal studies, the compound was successful when administered orally and intravenously or injected into the abdomen. In one experiment, mice given what should have been a fatal dose of multi-drug-resistant bacteria were rescued by the new compound.

The search for this compound took decades because of the specificity and safety required of the synthetic molecule.

Zhou credits his late colleague, former Duke Biochemistry Chair Christian Raetz, for starting the search decades ago. "He spent his entire career working on this pathway," Zhou said. "Dr. Raetz proposed a conceptual blueprint for this pathway in the 1980s, and it took him over two decades to identify all of the players," Zhou said.

The new drug's target is an enzyme called LpxC that is the second enzyme in the "Raetz pathway" and is essential to making the outer membrane lipid in gram-negative bacteria.

Raetz joined Duke as the chairman of biochemistry in 1993 after his work on this pathway at Merck & Co. had failed to produce a successful clinical candidate. The Merck antibiotic worked, but only against E. coli, so it wasn't commercially viable and the pharmaceutical company dropped it.

"He actually recruited me to Duke to work on this enzyme, initially just from the structural biology perspective," said Zhou, who came to Duke in 2001.

Zhou and Raetz had solved the structure of the LpxC enzyme and revealed molecular details of a few potential inhibitors. "We realized that we could tweak the compound to make it better," Zhou said. Since then, Zhou has been working with his colleague, Duke Chemistry professor Eric Toone, to make more potent LpxC inhibitors.

The first human trial of LpxC inhibitors had failed because of cardiovascular toxicity. The focus of the Duke group's subsequent work was to avoid cardiovascular effects while maintaining the potency of the compound.

They worked on more than 200 different versions of the enzyme inhibitor, always searching for better safety and more potency. Other compounds worked to varying degrees, but compound number 233 was the winner.

LPC-233 fits a binding spot on the LpxC enzyme and prevents it from doing its work. "It fits in the right way to inhibit formation of the lipid," Zhou said. "We're jamming the system."

Adding to its durability, the compound works by a remarkable two-step process, Zhou said. After the initial binding to LpxC, the enzyme-inhibitor complex changes its shape somewhat to become an even more stable complex.

The lifetime of the inhibitor binding in this more stable complex is longer than the lifetime of the bacteria. "We think that contributes to the potency, as it has a semi-permanent effect on the enzyme," he said. "Even after the unbound drug is metabolized by the body, the enzyme is still inhibited due to the extremely slow inhibitor dissociation process," Zhou said.

There are multiple patents being filed on the series of compounds, and Toone and Zhou have co-founded a company called Valanbio Therapeutics, Inc. which will be looking for partners to bring LPC-233 through phase 1 clinical trials to assess safety and efficacy in humans.

"All of these studies were done in animals," Zhou said. "Ultimately the cardiovascular safety needs to be tested in humans."

Large scale synthesis of LPC-233 was first accomplished by David Gooden at the Duke Small Molecule Synthesis Facility. Vance Fowler and Joshua Thaden (Duke School of Medicine), Ziqiang Guan (Biochemistry) and Ivan Spasojevic (Duke PK/PD Core) helped with in vivo studies, mass spectrometry and pharmacokinetics analysis.

More information: Jinshi Zhao et al, Preclinical Safety and Efficacy Characterization of an LpxC Inhibitor against Gram-negative Pathogens, Science Translational Medicine (2023). DOI: 10.1126/scitranslmed.adf5668. www.science.org/doi/10.1126/scitranslmed.adf5668

https://medicalxpress.com/news/2023-08-synthetic-antibiotic-effective-drug-resistant-superbugs.html#google_vignette

COVID-19 causes mitochondrial dysfunction in heart and other organs

 Since the beginning of the COVID-19 pandemic caused by the SARS-CoV-2 virus, researchers have been trying to determine why this virus creates such negative long-term effects compared with most coronaviruses.

Now, a multi-institutional consortium of researchers led by a team at Children's Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT) has found that the genes of the mitochondria, the energy producers of our cells, can be negatively impacted by the virus, leading to dysfunction in multiple organs beyond the lungs. These findings, published by the journal Science Translational Medicine, suggest new approaches for treating COVID-19.

Mitochondria are found in every cell in our bodies. The genes responsible for generating mitochondria are dispersed across both the nuclear DNA located in the nucleus of our cells and the mitochondrial DNA (mtDNA) located within each mitochondrion. Prior studies have shown that SARS-CoV-2 proteins can bind to mitochondrial proteins in host cells, potentially leading to mitochondrial dysfunction.

To understand how SARS-CoV-2 impacts mitochondria, researchers from the Center for Mitochondrial and Epigenomic Medicine (CMEM) at CHOP along with their COV-IRT colleagues wanted to analyze mitochondrial gene expression to detect differences caused by the virus. To do this, they analyzed a combination of nasopharyngeal and autopsy tissues from affected patients and animal models.

"The tissue samples from human patients allowed us to look at how mitochondrial gene expression was affected at the onset and end of disease progression, while animal models allowed us to fill in the blanks and look at the progression of gene expression differences over time," said the study's first author Joseph Guarnieri, Ph.D., a postdoctoral research fellow with the CMEM at CHOP.

The study found that in autopsy tissue, mitochondrial gene expression had recovered in the lungs, but mitochondrial function remained suppressed in the heart as well as the kidneys and liver. When studying animal models and measuring the time when the viral load was at its peak in the lungs, mitochondrial gene expression was suppressed in the cerebellum even though no SARS-CoV-2 was observed in the brain. Additional animal models revealed that during the mid-phase of SARS-CoV-2 infection, mitochondrial function in the lungs was beginning to recover.

Taken together, these results reveal that host cells respond to initial infection in a way that involves the lungs, but over time, mitochondrial function in the lungs is restored, while in other organs, particularly the heart, mitochondrial function remains impaired.

"This study provides us with strong evidence that we need to stop looking at COVID-19 as strictly an upper respiratory disease and start viewing it as a systemic disorder that impacts multiple organs," said co-senior author Douglas C. Wallace, Ph.D., director of the CMEM at CHOP. "The continued dysfunction we observed in organs other than the lungs suggests that mitochondrial dysfunction could be causing long-term damage to the internal organs of these patients."

While future studies using this data will study how systemic immune and inflammatory responses may be responsible for more severe disease in some patients, the research team did find a potential therapeutic target in microRNA 2392 (miR-2392), which was shown to regulate mitochondrial function in human tissue samples used in this study.

"This microRNA was upregulated in the blood of patients infected by SARS-CoV-2, which is not something we normally would expect to see," said co-senior author Afshin Beheshti, Ph.D., a biostatistician, a visiting researcher at The Broad Institute, and founder and President of COV-IRT. "Neutralizing this microRNA might be able to impede the replication of the virus, providing an additional therapeutic option for patients who are at risk for more serious complications related to the disease."

Next, Dr. Wallace and CMEM will conduct research into how mtDNA variation among world populations might affect mitochondrial function and thus individual sensitivity to SARS-CoV-2. According to Wallace, the demonstration that SARS-CoV-2 markedly affects mitochondrial function supports the hypothesis that individual differences in mitochondrial function could be a factor in individual severity of COVID-19.

More information: Joseph Guarnieri et al, Core mitochondrial genes are downregulated during SARS-CoV-2 infection of mammalian hosts, Science Translational Medicine (2023). DOI: 10.1126/scitranslmed.abq1533. www.science.org/doi/10.1126/scitranslmed.abq1533

https://medicalxpress.com/news/2023-08-covid-mitochondrial-dysfunction-heart.html

Brain mechanism that drives focus

 Trying to finish your homework while the big game is on TV? "Visual-movement" neurons in the front of your brain can help you stay focused, according to a new study from neuroscientists in the Perelman School of Medicine at the University of Pennsylvania.

In the study, published recently in Neuron, the scientists sought to illuminate the neural mechanism that helps the brain decide whether to focus visual attention on a rewarding task or an alluring distraction. By analyzing neuron activity in animal models as they faced this kind of attentional conflict, the researchers discovered that a pattern of coordinated activity called "beta bursts" in a set of neurons in the lateral prefrontal cortex (LPFC)—a section in the front of the brain responsible for motivation and rewards—appears to have a major role in keeping attention task-focused, essentially by suppressing the influence of the distracting stimulus.

"Our research suggests that while all brains have the ability to focus on a rewarding task and filter out distractions, some are better at it than others," said senior author Bijan Pesaran Ph.D., the Robert A Groff II Professor of Neurosurgery at Penn Medicine. "By understanding how our brains process rewarding stimuli, we hope to be able to also understand failures to do so in a variety of cognitive and psychiatric disorders, including attention deficit disorder, schizophrenia, and obsessive-compulsive disorder."

Humans and other large mammals can tune out distractions to keep their attention focused on actions that further goals. This is called "top-down" control, in which attention is directed towards a task with the intention of accomplishing a rewarding goal. Large mammals like primates also have brain circuitry that automatically redirects their attention based on incoming sights and sounds and other "salient" sensory stimuli, otherwise known as "bottom-up" control. How the brain suppresses such distractions to keep attention focused on a goal-related task has never been fully clear, until now.

In the new study, the researchers sought to understand what directs attention to some stimuli, but suppresses others in more detail. Using animal models, researchers recorded how activity in the LPFC shifts while completing a task and being presented with visual distractions. The neuroscientists found strong evidence that one specific type of LPFC neurons, called visual-movement neurons, direct attention towards either the rewarding shape or the distracting one.

The researchers also observed that visual-movement neurons in the LPFC fired together at the same frequency, called "beta bursts," during periods of focus (when ignoring visual distractions and completing tasks). When these beta bursts occurred in the moments before the visual stimuli were presented, subjects were far more likely to ignore the visual stimuli and complete the task. In contrast, when the beta bursts were weak or absent before visual stimuli were presented, subjects were more likely to move their attention to the bright but unrewarding shapes.

"This suggests to us that the beta-bursts originate in a network of visual-movement neurons, and act as 'traffic directors' for the neurons that process different visual stimuli," said first author Agrita Dubey, Ph.D., a postdoctoral researcher in the Pesaran laboratory. "It also suggests that focusing on a rewarding task takes a great deal of energy, and that it may be something that can be improved, especially in individuals with attention deficits."

More information: Agrita Dubey et al, Top-down control of exogenous attentional selection is mediated by beta coherence in prefrontal cortex, Neuron (2023). DOI: 10.1016/j.neuron.2023.06.025

https://medicalxpress.com/news/2023-08-neuroscientists-brain-mechanism-focus.html

RFK Jr. Exposes 'The Wuhan Cover Up'

 by Robert Malone via The Brownstone Institute,

The title of US Presidential candidate Robert F. Kennedy Jr.’s new book, The Wuhan Cover Up, does not really represent the scope and nature of this seminal work. 

This book is the most comprehensive historic summary and indictment of the history of the United States’ biowarfare/biodefense program ever written.

Summarizing an amazing sweep of untold censored history, it begins with ancient Mediterranean and European examples of both chemical and biological warfare, proceeds to an open discussion of the shocking truths concerning Imperial Japan’s WWII biowarfare program (Unit 731), the importation of both Japanese and German biowarfare experts and technologies into Fort Detrick to create USAMRIID (operation Paperclip), strategic evasion of global biowarfare “treaties,” through to the present Wuhan Institute of Virology CIA/Intelligence Community/Chinese CCP collusion and cover up, and concludes by glancing into the future.

What is often overlooked by academia, corporate media, and the Washington, DC political caste is that the history of modern biology (particularly microbiology, molecular biology, and virology) and the infectious disease pharmaceutical industry is intimately entwined with the American biowarfare enterprise. 

It has been estimated that total Federal expenditures on biowarfare research and development from the end of WWII through to the implementation of the Biological and Toxin Weapons Convention (1975) exceeded the costs of the US Nuclear Warfare program during this period, and this biowarfare program (and funding stream) is intimately linked to academia.  

Most of the leaders of the American Society of Microbiology were also leaders in the American DoD/CIA-funded biowarfare program.  This background and context is necessary to understand how the fundamental corruption of academic medicine, peer-reviewed journals, the CDC, FDA, biological and academic research have been so comprehensive, as has been revealed by the COVID crisis. 

Just follow the money.

Which leads us to the most recent and egregious sordid chapter in this sorry tale, The Wuhan Cover Up. 

A case study demonstrating the consequences of the situational ethical slide which often occurs when a massive administrative bureaucracy fuses with an “intelligence community.” 

The resulting Leviathan, steeped in the utilitarian “ends justify the means” logic typical of all those skilled liars who have practiced spycraft throughout the ages, eventually forgets both its purpose and its commitment to serving the citizenry, and becomes a predatory monster. 

With his masterful summary, Mr. Kennedy has provided the receipts on how this modern embodiment of the slouching beast foretold in Yeats’ “Second Coming” has been born and nurtured via a cooperation of convenience between the Western and Eastern military/intelligence/industrial complexes. 

Now, looking forward, the open question is whether this globalized Leviathan will continue to succeed in its efforts to deploy advanced psychological and information control methods on the entire human community to avoid the consequences of its actions?

Or will this book and the work of so many others trigger an awareness, awakening, and effective reaction among citizens to the deep corruption of medical-biological research, medical ethics, and the entire Western “health” enterprise which has occurred over the last century? 

With this book as a guide, we can see the enemy, the face of creeping globalized utilitarian evil, and it is us

https://www.zerohedge.com/political/rfk-jr-exposes-wuhan-cover