Take it away Gary..

Hi Penny:

   With respect to the E. coli in preschools in Calgary, one might ask what is the source of the E. coli O157:H7 and how does it get into the environment? It turns out that stopping the production of E. coli O157:H7 and other acid resistant E. coli is as simple as no longer feeding beef and diary cattle the high production diet containing corn. This problem is pervasive in agriculture as the common goal in agriculture is to maximize yield in order to maximize profit. The scientific evidence to support my statement is found here:

Gary’s okay and further comment

Certainly go ahead and share the blog. I have never seen the mainstream media mention it. One way to fool the public is to withhold information. The MSM is good at that.

You are right, cattle should eat grass. Corn fattens cattle because of what is and isn’t in the corn. Corn is lacking in three essential amino acids, methionine, tryptophan and lysine. Thus feeding corn to cattle results in their being malnourished so they keep eating the corn to try to meet their nutritional need. In so doing, the excess carbohydrate fattens them. It does the same to people. Hybrid corn does a better job as it has more carbohydrate and less protein. The reason for hybrid corn is higher yield and the consequence is reduced nutritional value.

Before we get to the info it’s worth noting- Gary is correct! I can’t recall ever seeing this information in the main stream media. We, hubby and myself, read about this type of stuff. In books. Since this is a topic that interests the both of us. Rather than preventing E. Coli contamintion what we largely get are new antibiotic and other pharma treatments. For profit, of course! But never a word on preventing or reducing this problem

Also, notice the E. Coli contamination is being used to score cheap political points against the government of the day, rather than actually caring about this serious problem

Idiotic Globe and Mail piece– Danielle Smith must uncover roots of E. coli crisis and ensure it doesn’t happen again

We already know what the roots are of this problem- This problem long predates Danielle Smith. But, she’s certainly the convenient scape goat – Notice the piece from Cornell was published in 1998

Simple change in cattle diets could cut E. coli infection

A simple change in cattle diets in the days before slaughter may reduce the risk of Escherichia coli (E. coli) infections in humans, U.S. Department of Agriculture (USDA) and Cornell University microbiologists have discovered.

Research reported in the Sept. 11 issue of the journal Science indicates that grain-based cattle diets promote the growth of E. coli that can survive the acidity of the human stomach and cause intestinal illness. E. coli contamination is responsible for more than 20,000 infections and 200 deaths each year in the United States.

Fortunately there is a workable solution to the food-safety problem, the scientists say. By feeding hay to cattle for about five days before slaughter, the number of acid-resistant E. coli can be dramatically reduced.

“Most bacteria are killed by the acid of stomach juice, but E. coli from grain-fed cattle are resistant to strong acids,” explains James B. Russell, a USDA microbiologist and faculty member of the Cornell Section of Microbiology. “When people eat foods contaminated with acid-resistant E. coli — including pathogenic strains like O157:H7 — the chance of getting sick increases.”

E. coli is a normal bacterium in the gastrointestinal tract of animals and humans, and most types are not harmful (See “E. coli and Cattle” fact sheet, attached). However, disease-causing strains such as E. coli O157:H7 produce toxins that cause bloody diarrhea or even kidney failure in humans. Mature cattle are unaffected by E. coli O157:H7. Only a small number of cattle (estimated at 1 to 2 percent at any one time) shed E. coli O157:H7 in their feces, a rate that is not fully explained.

When beef carcasses are accidentally contaminated by feces at slaughter, the pathogens can enter the human food supply. E. coli O157:H7 can be killed by cooking or irradiation, but the bacterium continues to pose a food-safety risk.

Cattle are fed starch-containing grains to increase growth rate and produce tender meat. Because the bovine gastrointestinal tract digests starch poorly, Russell explains, some undigested grain reaches the colon, where it is fermented. When the grain ferments — and acetic, propionic and butyric acids accumulate in the animal’s colon — a large fraction of E. coli produced are the acid-resistant type.

“Grain does not specifically promote the growth of E. coli O157:H7, but it increases the chance that at least some E. coli could pass through the gastric stomach of humans,” Russell says. “The carbohydrates of hay are not so easily fermented, and hay does not promote either the growth or acid resistance of E. coli. When we switched cattle from grain-based diets to hay for only five days, acid-resistant E. coli could no longer be detected.”

In studies performed at Cornell, beef cattle fed grain-based rations typical of commercial feedlots had 1 million acid-resistant E. coli, per gram of feces, and dairy cattle fed only 60 percent grain also had high numbers of acid-resistant bacteria. In each case, the high counts could be explained by grain fermentation in the intestines.

By comparison, cattle fed hay or grass had only acid-sensitive E. coli, and these bacteria were destroyed by an “acid shock” that mimicked the human stomach, the microbiologists report in Science.

According to microbiologist Russell, acid-resistant strains of bacteria have evolved to overcome the protective barrier of the gastric stomach. The ongoing process of natural selection allows organisms with the appropriate genes to survive and multiply where others cannot. Because cattle have been fed high-grain, growth-promoting diets for more than 40 years, he says, there has been ample opportunity to select acid-resistant forms.

Further research is needed to identify the acid-resistance genes of E. coli, but Russell says that “common laboratory strains” of E. coli appear to lack the necessary DNA to survive acidic gastrointestinal environments.

“In the meantime, now that we know where the acid-resistant E. coli are coming from, we can control them with a relatively inexpensive change in diet,” Russell says. “This strategy has the potential to control the production of other acid-resistant bacteria, including virulent strains of E. coli that have not yet evolved.”

A brief period of hay-feeding immediately before slaughter “should not affect either carcass size or meat quality,” and the diet change could be implemented with minimal expense and inconvenience to feedlot operators, according to Donald H. Beermann, Cornell professor of animal science.

USDA microbiologist Russell has been stationed in Ithaca for more than 17 years and is affiliated with the U.S. Dairy Forage Research Center in Madison, Wisc. He holds the rank of adjunct professor of microbiology at Cornell, and the other authors of the Science report were his students when the feeding studies were conducted: Francisco Diez-Gonzalez, currently a postdoctoral fellow, completed his Ph.D. in food science at Cornell in 1996. Todd Callaway is a Ph.D. candidate in microbiology. Menas Kizoulis, a Cornell senior in biological sciences, was recently awarded a Howard Hughes Undergraduate Fellowship to continue research in Russell’s laboratory.

An article from Mother Earth News

E. coli 0157:H7, the toxic strain that caused the recent outbreak of food poisoning from bagged spinach, is a fairly recent discovery; it was unknown before 1982

One of the reasons this new strain makes us sick is that it is more acid-resistant than other forms of E. coli, so it can pass through our stomachs unharmed into the intestines, where it produces a toxin that causes diarrhea and organ damage. So, how did an acid-resistant strain of E. coli develop? Most outbreaks have been linked to cattle, and one major change in beef production in recent decades has been the confinement of cattle to feedlots where they are fed high-grain diets. It is now clear that forcing cattle to eat an unnatural high-grain diet, rather than their natural diet of grass, isn’t good for the cows, or for us. Here’s how Michael Pollan explains it in his brilliant new book, The Omnivore’s Dilemma:

When I was young, not to sound cheesy, but meat tasted completely different and never did I hear a peep about e coli– Nadda! Until I was in my ’20’s.

https://hms.harvard.edu/news/when-comes-immunity-you-are-what-you-eat

Research in mice shows gut bacteria feed on common fatty acids, and the byproduct of this process stimulates the rise of immune cells in the gut.
Immune cascade spurred by fatty acid consumption shielded the mice against disease-causing gut bacteria.
Study offers striking demonstration of how diet and gut microbes work together to build the human immune system.

The notion that diet and health are inextricably linked is hardly novel. For millennia, people have known that poor nutrition is responsible for many health problems. But the precise mechanisms that explain just how diet alters the function of our cells, tissues, and organs have remained poorly understood.

People knew this? Did they forget it during Covid? How would or could they have forgotten what humanity has known for millennia? Oh, yes, the lying media convinced them otherwise!

The findings, the team said, detail an intricate interplay between gut microbes, food, and immunity. They also underscore the importance of understanding how individual microbial species in the gut could alter specific organ functions and exercise important effects on health.

“The triad of diet-microbes-immune system has attracted considerable attention, with a paucity of detail to demonstrate how these three components work together,” said study senior author Dennis Kasper, the William Ellery Channing Professor of Medicine at Brigham and Women’s Hospital and professor of immunology in the Blavatnik Institute at Harvard Medical School. “We have found one of the clearest demonstrations here of a mechanism underlying how diet and the microbiome build the immune system.”

We already know this! And as a species we’ve long known this. Only because of our sick societal encouraged disconnect from reality can we be convinced otherwise

CNN

The US Food and Drug Administration has given a safety clearance to lab-grown meat for the first time.

“The FDA’s goal is to support innovation in food technologies while always maintaining as our first priority the safety of the foods available to U.S. consumers,” the statement added.

The FDA’s goal is to support innovation that can be patented for mass profit

Upside Foods did not immediately respond to a request for comment but company founder and CEO Uma Valeti said on Twitter that its cultivated chicken “was one step closer to being on tables everywhere.”

“UPSIDE has received our ‘No Questions Letter’ from the FDA,” Valeti tweeted. “They’ve accepted our conclusion that our cultivated chicken is safe to eat.”

Let me repeat the above quote;

The FDA accepted the food manufacturers conclusion that cultivated chicken is safe to eat. FDA rubber stamps (a person or organization that gives automatic approval or authorization to the decisions of others, without proper consideration.) faux food.

And a hit for terrain theory - By using the antibiotics, thereby altering the terrain of individuals given anti biotics organ failure and death occurred.

https://www.newswise.com/articles/certain-antibiotics-are-associated-with-an-increased-risk-of-mortality-in-critically-ill-patients

ANN ARBOR, MI – A common clinical practice may be inadvertently harming patients, according to new research published October 13 in the European Respiratory Journal. The team of Michigan Medicine researchers behind the study suggest that administration of antibiotics with activity against anaerobic bacteria has a profound effect on the gut microbiome and, ultimately, an adverse impact on critically ill patients.

“We talk about the gut microbiome as a metabolic and immune ‘organ,’ and when we give patients anti-anerobic antibiotics, I worry we are causing a hidden form of organ failure,” said senior author Robert Dickson, M.D., Associate Professor in Pulmonary and Critical Care Medicine and Deputy Director at the Weil Institute for Critical Care Research and Innovation at the University of Michigan. “Our research suggests that depleting the gut of these ‘good bugs’ may be contributing to worse clinical outcomes.”

Honestly, I thought this has been known for years. Example antibiotics for a recent dental surgery result in an increased intake in live culture foods- You can ferment your own food very easily.

What was unknown to me is how this causes organ failure and death!

In the paper, researchers found that, in critically ill patients, the practice of early administration of anti-anaerobic antibiotics is commonplace – about two-thirds of the 3,032 patients observed in the study’s cohort received such treatment.

“For sick patients in the Emergency Department and Intensive Care Unit, there has been a lot of focus on ‘time-to-antibiotics’ as a quality improvement measure,” said Dickson. “Our results demonstrate that antibiotics really can’t be considered a single entity, as they have widely different impacts on the microbiome and on our patients. Patients who received anti-anaerobic antibiotics did far worse than patients who didn’t. We think that which antibiotic is given probably matters more than how quickly they are administered.”

With support from the Weil Institute, along with funding from the National Institutes of Health, the researchers conducted a retrospective single-center cohort study of 3,032 critically ill patients, comparing those who did and did not receive early anti-anaerobic antibiotics. By comparing ICU outcomes in all patients, and changes in gut microbiota in 116 of the patients, they found that those who received anti-anaerobic antibiotics early in their hospital course had worse outcomes, whether measured in overall survival, infection-free survival, or pneumonia-free survival.

The authors also found dramatic consequences of these antibiotics on the gut microbiome – during hospitalization, patients who received anti-anaerobic antibiotics had decreased initial gut bacterial density, followed by increased expansion and domination of the microbiome Enterobacteriaceae (a genus of common bacteria, many of which are pathogenic and cause opportunistic infections in immunocompromised hosts). These findings confirm that anti-anaerobic antibiotics have a dramatic effect on gut bacterial communities.

While the primary findings were from an observational study in humans, the team confirmed the results using animal modeling. In two different mouse models (pneumonia and oxygen-induced lung injury), animals who were treated with anti-anaerobic antibiotics did worse. Anti-anaerobic antibiotics increased the susceptibility of mice to pneumonia due to Enterobacteriaceae and increased their mortality from oxygen toxicity.

Co-author Rishi Chanderraj, M.D., a Clinical Lecturer in Infectious Diseases at U-M, was the lead researcher on the initial project and will be carrying the work forward in future studies.

“In observational studies, there is always a risk that a mortality difference is due to confounding; maybe the patients who received anti-anaerobic antibiotics were just sicker,” he said. “But the fact that we were able to recapitulate these findings in two different animal models gives us confidence that these findings are real.”

“No one wants to withhold antibiotics from patients with life-threatening infections,” said Chanderraj. “But our study confirms that the risk of overtreating with antibiotics isn’t just theoretical. I’m concerned that we’re harming our patients.”

#

Paper cited: “In critically ill patients, anti-anaerobic antibiotics increase risk of adverse clinical outcomes,” European Respiratory Journal. DOI: 10.1183/13993003.00910-2022

Project team: Rishi Chanderraj1,2, Jennifer M. Baker3,4, Stephen G. Kay3, Christopher A. Brown3,5, Kevin J. Hinkle3, Daniel J. Fergle3, Roderick A. McDonald3, Nicole R. Falkowski3, Joseph D. Metcalf3, Keith S. Kaye6, Robert J. Woods1,2,7, Hallie C. Prescott3,8,9, Michael W. Sjoding3,7,8,10, Robert P. Dickson3,4,10

Affiliations:

Division of Infectious Diseases, Department of Internal Medicine, University of Michigan

Medical School, Ann Arbor, MI, USA.

Medicine Service, Infectious Diseases Section, Veterans Affairs (VA) Ann Arbor Healthcare

System, Ann Arbor, Michigan, USA.

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine,

University of Michigan Medical School, Ann Arbor, MI, USA.

Department of Microbiology and Immunology, University of Michigan Medical School, Ann

Arbor, MI, USA.

Institute for Research on Innovation and Science, Institute for Social Research, University of

Michigan

Division of Infectious Diseases, Department of Medicine, Rutgers-New Jersey Medical

School

Computational Medicine and Bioinformatics, University of Michigan Medical School, Ann

Arbor, MI, USA.

Institute for Healthcare Policy and Innovation, University of Michigan, Ann Arbor, Michigan.
VA Center for Clinical Management Research, Ann Arbor, Michigan.
Weil Institute for Critical Care Research & Innovation; Ann Arbor, Michigan

EWG

A draft World Health Organization analysis of the two most notorious “forever chemicals” disregards hundreds of health risk studies, claiming there are too many uncertainties to calculate a safe exposure level for the substances.

The two chemicals are PFOA, formerly used by DuPont to make Teflon, and PFOS, formerly an ingredient in 3M’s Scotchgard, both members of the class of per- and polyfluoroalkyl substances, or PFAS.

The draft

“Background document for development of WHO Guidelines for Drinking-water Quality,” disregards WHO’s mission of putting public health first: It creates the potential for doubt about how PFOA and PFOS harm people. Instead, WHO emphasizes cutting the cost of removing the chemicals from water.

Across the globe, PFAS exposure is an urgent public health priority. Decades of widespread PFAS use have contaminated water, soil and animals in the farthest corners of the world. Today PFAS are found in the blood of virtually everyone, including newborn babies who are exposed when PFAS cross from the pregnant body to cord blood.

We know very low doses of PFAS have been linked to suppression of the immune system, including reduced vaccine efficacy. These chemicals harm development and the reproductive system, such as reduced birth weight and impacts on fertility; increase the risk of certain cancers; and affect metabolism, such as changes in cholesterol and weight gain.

The Environmental Protection Agency acknowledges these risks, recently proposing significantly stricter but non-binding advisories for levels of PFOA and PFOS in drinking water above which health harms could be expected following a lifetime of exposure.

The WHO draft sows unnecessary doubt where hard facts already exist. It resembles the tobacco and chemical industry playbook – raising already answered questions about legitimate scientific studies to create confusion over the risks of a particular substance. The draft says there are too many uncertainties about the science on PFOA and PFOS to know what level of exposure might be considered safe.

There are several aspects of the WHO report that are flawed and do not follow established risk assessment guidelines, leaving public health unprotected.

Instead of focusing on the health risks of PFAS, the WHO prioritizes discussion about how to minimize the cost of removing forever chemicals from contaminated water. This approach protects the polluting industries that have discharged PFAS for decades.

Not the least bit surprising coming from the WHO!

WHO is taking public comments on the draft document until November 11. A strong, unified response from public health advocates outlining the problems with the report is essential to correcting its numerous flaws and omissions. Only with these fixes can the report help ensure that health protection from PFAS stays a priority.

Bechampe’s book

Bechamp or Pasteur?: A Lost Chapter in the History of Biology

Oh and Pasteur is clearly a fraudster though definitely a darling of the political elites- Think of Fauci at this time and you’ll ‘get’ the infamy of Pasteur in his day

R. Pearson’s Pasteur, Plagiarist, Imposter, originally published in 1942, serves as the introduction. It details some of the reasons for the rancorous relationship between Louis Pasteur and Antoine Béchamp. Pearson points out many of the problems in Pasteur’s work, and provides details, statistics and evidence to support his case. Some of the frauds which were eventually admitted by the Pasteur Institute are mentioned here.

Consider the reality, the obvious reality, that our microbiome is being damaged by our disgusting western diet/lifestyle. This damage is leaving us sicker. Our increased dis-ease is leaving us all as victims to the depredation (an act of attacking or plundering) of the elite classes.

Humans evolved with their microbiomes and this microbiome pass from generation to generation

When the first humans moved out of Africa, they carried their gut microbes with them. Turns out, these microbes also evolved along with them.

The human gut microbiome is made up of hundreds to thousands of species of bacteria and archaea. Within a given species of microbe, different strains carry different genes that can affect your health and the diseases you’re susceptible to.

There is pronounced variation in the microbial composition and diversity of the gut microbiome between people living in different countries around the world. Although researchers are starting to understand what factors affect microbiome composition, such as diet, there is still limited understanding on why different groups have different strains of the same species of microbes in their guts.

Microbes share evolutionary history with humans (of course they do!)

We hypothesized that as humans fanned out across the globe and diversified genetically, so did the microbial species in their guts. In other words, gut microbes and their human hosts “codiversified” and evolved together – just as human beings diversified so that people in Asia look different from people in Europe, so too did their microbiomes.

Oh, so people are truly different? That is such a non woke statement. Though it’s just stating the obvious.

To assess this, we needed to pair human genome and microbiome data from people around the world. However, data sets that provided both the microbiome data and genome information for individuals were limited when we started this study. Most publicly available data was from North America and Western Europe, and we needed data that was more representative of populations around the world.

So our research team used existing data from Cameroon, South Korea and the United Kingdom, and additionally recruited mothers and their young children in Gabon, Vietnam and Germany. We collected saliva samples from the adults to ascertain their genotype, or genetic characteristics, and fecal samples to sequence the genomes of their gut microbes.

For our analysis, we used data from 839 adults and 386 children. To assess the evolutionary histories of humans and gut microbes, we created phylogenetic trees for each person and as well as for 59 strains of the most commonly shared microbial species.

When we compared the human trees to the microbial trees, we discovered a gradient of how well they matched. Some bacterial trees didn’t match the human trees at all, while some matched very well, indicating that these species codiversified with humans. Some microbial species, in fact, have been along for the evolutionary ride for over hundreds of thousands of years.

The human gut microbiome is made up of hundreds to thousands of species of bacteria and archaea. Within a given species of microbe, different strains carry different genes that can affect your health and the diseases you’re susceptible to.

There is pronounced variation in the microbial composition and diversity of the gut microbiome between people living in different countries around the world. Although researchers are starting to understand what factors affect microbiome composition, such as diet, there is still limited understanding on why different groups have different strains of the same species of microbes in their guts.

Our discovery that gut microbes evolved right along with their human hosts offers another way to view the human gut microbiome. Gut microbes have passed between people over hundreds to thousands of generations, such that as humans changed, so did their gut microbes.

Or as the gut microbes changed the people changed?

As a result, some gut microbes behave as though they are part of the human genome: They are packages of genes that are passed between generations and shared by related individuals. ( Part of Bechampe’s theory)

Of course the idea here is to create personalized, for profit, medicine.

My idea has more to do with eating better quality, nutritious food. Eschew the junk. And nothing lab created. Nothing!

Linked here but originating with Endocrine Society

Prenatal exposure to endocrine-disrupting chemicals found in everyday products may interfere with the developing offspring’s brain, according to a rat study being presented Monday at ENDO 2022, the Endocrine Society’s annual meeting in Atlanta, Ga.

P.S. MohanKumar, Ph.D., professor at the University of Georgia in Athens, Ga., and colleagues, focused on the gestational effects of endocrine-disrupting chemicals bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP), and if they would change stress-related behaviors.

“This research is significant because prenatal exposure to these chemicals may contribute to mood disorders later in life,” said study co-author Amrita Kaimal, Ph.D., of the University of Georgia Neuroscience Graduate Program.

A total of 76 Sprague-Dawley rats were used for the study. After the rats were mated, pregnant female rats were administered oral saline, BPA, a combination of BPA and low-dose DEHP, or a combination of BPA and high-dose DEHP during days 6-21 of pregnancy. All of the doses were adjusted according to the body weight of the rat.

Behavioral tests were conducted in adult offspring, and brains from the rats were analyzed for monoamine neurotransmitters, like dopamine and serotonin.

Female offspring administered BPA and a combination of BPA and low-dose DEHP displayed less anxiety in the Open Field Test, which measures activity and exploratory behavior. However, male offspring administered high-dose DEHP showed feminized anxiety-like behavior in a maze. Fear responses among male offspring in most of the groups exposed to endocrine-disrupting chemicals were impaired in a test examining the response to a threatening object. Interestingly, low-dose endocrine disruptors led to passive coping strategies in male and female offspring.

Brain studies indicate male offspring in the BPA, low-dose and high-dose DEHP, and BPA and high-dose DEHP groups had diminished dopamine levels in the paraventricular hypothalamic nucleus. This is associated with their impaired fear response.

“Our study confirms sex-specific behavioral changes in offspring as a result of these exposures, highlighting the fact that exposure to these chemicals should be avoided during pregnancy,” MohanKumar said.

MohanKumar will present at the Society’s ENDO 2022 endocrine-disrupting chemicals news conference at noon on Saturday, June 11. Register to attend the news conference at www.endowebcasting.com.