FatBuster Bacteria Frequencies

Stomach bug makes food yield more calories

Mice with a hefty dose of a certain gut bacteria are fatter.
by Helen Pearson, May 26, 2006
[email protected]

Scientists have identified a key microbe in our guts that helps us glean more calories from food. The discovery backs the idea that the type of microbes in our gut help to determine how much weight we gain, and that seeding the intestine with particular bugs could help fight obesity…

The researchers took mice that had been grown in a sterile environment, with no microbes in their guts, and injected them with a very common strain of human intestinal bacteria, called Bacteroides thetaiotaomicron. Some of the mice also received a dose of of M. smithii.

About 100 times more microorganisms took up residence in the colon of mice injected with both B. theta and M. smithii than in those injected with B. theta alone. This suggests that the presence of waste-removing M. smithii was somehow helping other bacteria to thrive. “There’s something cool going on,” Buck says.

When both microbes were present, B. theta boosted the activity of genes involved in breaking down and metabolizing fructans a food component common in onions, wheat and asparagus that the human gut cannot digest by itself. B. theta converted the fructans into fatty acids, some of which were taken up by the mouse gut and either used as fuel or stored as fat.

In humans, around 10% of our calories come from such microbe-manufactured fatty acids. After a few weeks, mice with both types of microbe had approximately 40% more of a particular fatty acid called acetate in their blood, and carried 15% more fat.

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Gut Bacteria Can Help Make You Fat or Thin

Health »

Scientific American Volume 310, Issue 6

» The Science of Health

See Inside

How Gut Bacteria Help Make Us Fat and Thin

Intestinal bacteria may help determine whether we are lean or obese

Jun 1, 2014 |By Claudia Wallis

For the 35 percent of American adults who do daily battle with obesity, the main causes of their condition are all too familiar: an unhealthy diet, a sedentary lifestyle and perhaps some unlucky genes. In recent years, however, researchers have become increasingly convinced that important hidden players literally lurk in human bowels: billions on billions of gut microbes.

Throughout our evolutionary history, the microscopic denizens of our intestines have helped us break down tough plant fibers in exchange for the privilege of living in such a nutritious broth. Yet their roles appear to extend beyond digestion. New evidence indicates that gut bacteria alter the way we store fat, how we balance levels of glucose in the blood, and how we respond to hormones that make us feel hungry or full. The wrong mix of microbes, it seems, can help set the stage for obesity and diabetes from the moment of birth.

Fortunately, researchers are beginning to understand the differences between the wrong mix and a healthy one, as well as the specific factors that shape those differences. They hope to learn how to cultivate this inner ecosystem in ways that could prevent—and possibly treat—obesity, which doctors define as having a particular ratio of height and weight, known as the body mass index, that is greater than 30. Imagine, for example, foods, baby formulas or supplements devised to promote virtuous microbes while suppressing the harmful types. “We need to think about designing foods from the inside out,” suggests Jeffrey Gordon of Washington University in St. Louis. Keeping our gut microbes happy could be the elusive secret to weight control.

Microbial ecology: human gut microbes associated with obesity.

Ley RE1, Turnbaugh PJ, Klein S, Gordon JI.

Author information

Abstract

Two groups of beneficial bacteria are dominant in the human gut, the Bacteroidetes and the Firmicutes. Here we show that the relative proportion of Bacteroidetes is decreased in obese people by comparison with lean people, and that this proportion increases with weight loss on two types of low-calorie diet. Our findings indicate that obesity has a microbial component, which might have potential therapeutic implications.

Comment in

Physiology: obesity and gut flora. [Nature. 2006]

PMID:

17183309

[PubMed – indexed for MEDLINE]

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Frequency subscribers have access to programs that eliminate pathogens known to be associated with obesity like crAssphage gut virus and

FatBuster Research Update: Fat Cell Apoptosis

librarie.immateriel.fr

Diet and exercise help remove fat but are not the root cause of the fat. Particularly as you get older fat accumulates in the abdomen while diet and exercise are increasingly less effective. Experimentation with fatbuster frequencies over the years has been helpful as frequencies in the 3mhz range appear to affect ribosomes that trigger fat cell death.

Recently, these frequencies have been found to be part of frequency sets for biofilms. Also the fat buildup in liposomes has bacterial infection in chronic fat tissue. The combination of precise targeting of the 3mhz frequency in the biofilm set combined with running the biofilm set at the same time works better than either one alone at dealing with fat. Biofilm frequencies are available to Frequency Research Foundation subscribers.

Fat buildup is related to disrupted hormone production in the body so a key dietary supplement, fish oil, is recommended. Carefully study of Dr. Barry Sears most recent book on “Toxic Fat Syndrome” show that factors in our food chain are systematically distorting hormone production and leading to the epidemics of diabetes and obesity. This can be the basis of a strategy to work systematically on the problem.

1. Daily work with the appropriate frequencies.

2. Balance protein and carbohydrate intake – the Zone Diet is not a diet, it is a hormone balancing system.

2. Take large amounts of molecularly distilled fish oil. Dr. Sears oil is recommended as it has synergistic natural compounds. Start with 4 grams in the morning and 4 at night to achieve the blood test results he recommends.

There are many papers in PubMed relating ribosome activity to cell apoptosis. For example:

Ribosome-inactivating protein and apoptosis: abrin causes cell death via mitochondrial pathway in Jurkat cells.

Sriram Narayanan

Avadhesha Surolia

Anjali A Karande

Molecular Biophysics Unit, Indian Institute of Science, Bangalore 560012, India.

Biochemical Journal (Impact Factor: 4.65). 02/2004; 377(Pt 1):233-40. DOI: 10.1042/BJ20030797

Source: PubMed

ABSTRACT Abrin belongs to the type II family of ribosome-inactivating proteins comprising a galactose-binding B chain coupled with a toxic A chain through a single disulphide linkage. Apart from its RNA-N-glycosidase activity, another role that has been recently ascribed to abrin was the induction of apoptosis. Studies were undertaken to determine the kinetics of these two activities. In the present study, we report that the signal for apoptosis is triggered at a time point later than the inhibition of protein synthesis. This apoptotic pathway induced by abrin is caspase 3-dependent but caspase 8-independent and involves mitochondrial membrane potential damage and reactive oxygen species production. Overexpression of B-cell lymphocytic-leukaemia proto-oncogene 2 was found to block this apoptotic pathway.

British Medical Journal Reports Cholesterol is Not the Issue, Low Saturated Fat is the Problem

OBSERVATIONS

From the Heart

Saturated fat is not the major issue

BMJ 2013; 347 doi: http://dx.doi.org/10.1136/bmj.f6340 (Published 22 October 2013)
Cite this as: BMJ 2013;347:f6340
Aseem Malhotra, interventional cardiology specialist registrar, Croydon University Hospital, London
[email protected]
Let’s bust the myth of its role in heart disease
Scientists universally accept that trans fats—found in many fast foods, bakery products, and margarines—increase the risk of cardiovascular disease through inflammatory processes. But “saturated fat” is another story. The mantra that saturated fat must be removed to reduce the risk of cardiovascular disease has dominated dietary advice and guidelines for almost four decades.
Yet scientific evidence shows that this advice has, paradoxically, increased our cardiovascular risks. Furthermore, the government’s obsession with levels of total cholesterol, which has led to the overmedication of millions of people with statins, has diverted our attention from the more egregious risk factor of atherogenic dyslipidaemia.
Saturated fat has been demonised ever since Ancel Keys’s landmark “seven countries” study in 1970. This concluded that a correlation existed between the incidence of coronary heart disease and total cholesterol concentrations, which then correlated with the proportion of energy provided by saturated fat. But correlation is not causation. Nevertheless, we were advised to cut fat intake to 30% of total energy and saturated fat to 10%.” The aspect of dietary saturated fat that is believed to have the greatest influence on cardiovascular risk is elevated concentrations of low density lipoprotein (LDL) cholesterol. Yet the reduction in LDL cholesterol from reducing saturated fat intake seems to be specific to large, buoyant (type A) LDL particles, when in fact it is the small, dense (type B) particles (responsive …
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As a medical school professor, I never bought in to the low fat myth. After decades of frequency work, I have concluded that my cholesterol which tends to be high is cause by infection induced inflammation by parasites circulating particularly with the swine flu, but even more important by biofilms which start in the gums and then spread throughout the body. The relation of biofilms to heart disease has been reported in a previous blog posting.
The Frequency Research Foundation has developed frequency sequences for almost 400 strains of periodontal biofilms. Over 600 strains have been DNA sequenced at the National Institute of Health. A large number of these strains are borrelia based lyme pathogens found in persons exposed to lyme organisms. These tend to cause high blood pressure as well as elevated cholesterol.

American Journal of Medicine Investigates “Chicken” Nuggets

The Autopsy of Chicken Nuggets Reads “Chicken Little”

Richard D. deShazo, MD

Steven Bigler, MD

Leigh Baldwin Skipworth, BA

published online 13 September 2013.
Corrected Proof

Abstract

Purpose

To determine the contents of chicken nuggets from 2 national food chains.

Background

Chicken nuggets have become a major component of the American diet. We sought to determine the current composition of this highly processed food.

Methods

Randomly selected nuggets from 2 different national fast food chains were fixed in formalin, sectioned and stained for microscopic analysis.

Results

Striated muscle (chicken meat) was not the predominate component in either nugget. Fat was present in equal or greater quantities along with epithelium, bone, nerve, and connective tissue.

Conclusion

Chicken nuggets are mostly fat, and their name is a misnomer.

Stomach bug makes food yield more calories

Mice with a hefty dose of a certain gut bacteria are fatter. by Helen Pearson, May 26, 2006 [email protected]

Microbial ecology: human gut microbes associated with obesity.

Author information

Abstract

Comment in

Ribosome-inactivating protein and apoptosis: abrin causes cell death via mitochondrial pathway in Jurkat cells.

OBSERVATIONS

From the Heart

Saturated fat is not the major issue

The Autopsy of Chicken Nuggets Reads “Chicken Little”

Abstract

Purpose

Background

Methods

Results

Conclusion

Mice with a hefty dose of a certain gut bacteria are fatter.
by Helen Pearson, May 26, 2006
[email protected]