Artificial sweeteners may lead to diabetes

Reaching for artificial sweeteners to avoid sugar may be trading one evil for another, a new study suggests.

For some people, artificial sweeteners may lead to type 2 diabetes as directly as eating sugar does, according to the research, published Wednesday in the journal Nature.

AP Artificial Sweeteners

The benefits and risks of artificial sweeteners have been debated for decades. Some studies show no link to diabetes and others suggest there is one. The new research, from the Weizmann Institute of Science in Israel, finds that differences in gut microbes may explain why some people can handle artificial sweeteners just fine while in an unknown percentage of others the sweeteners lead to diabetes.

The human digestive system is home to millions of microbes, largely bacteria, that help digest food and may play a role in health.

The researchers were quick to note that their work needs to be repeated before it’s clear whether artificial sweeteners truly can trigger diabetes.

“I think this issue is far from being resolved,” said Eran Elinav, who studies the link between an individual’s immune system, gut microbes and health at the Weizmann Institute.

He admitted that his research has soured him on sweetening the coffee he needs to get through his day.

“I’ve consumed very large amounts of coffee and extensively used sweeteners, thinking that they were at least not harmful and perhaps even beneficial,” Elinav said at a telephone news conference Tuesday. “Given the surprising result we got in our study, I made a decision to stop using” artificial sweeteners.

George King, chief scientific officer at the Joslin Diabetes Center in Boston, who wrote the forthcoming book The Diabetes Reset, said he may start cutting back on his diet soda habit, too.

“I think I will recommend that people not drink more than one or two cans a day,” said King, who was not involved in the new research.

Artificial sweeteners cannot be digested, so it was assumed that there would be no way for them to lead to diabetes. Microbes seem to provide the missing link.

In a series of experiments in mice and people, the researchers examined the interaction between gut microbes and consumption of the sweeteners aspartame, sucralose and saccharine. Depending on the types of microbes they had in their intestines, some people and mice saw a two- to fourfold increase in blood sugars after consuming the artificial sweeteners for a short time. Over time, high blood sugar levels can lead to diabetes.

“The magnitude of the differences were not just a few percentages. These were actually very dramatic differences we saw both in the mice and in the human settings,” said Eran Segal, a study co-author who is a computational biologist at the Weizmann Institute.

The study involved several parts:

• A diet study of 400 people found that those who consumed the most artificial sweeteners were more likely to have problems controlling blood sugar.

• Seven people who did not normally consume artificial sweeteners were followed intensively over a week as they were fed controlled amounts of saccharine. Four of the seven showed significant increases in blood sugar levels.

• Mice fed the sweetener saccharine saw dramatic increases in their blood sugar levels.

• Mice with no gut microbes did not see increases in blood sugar levels when they ate artificial sweeteners. Once these bug-free mice were treated with the feces of normal mice that had eaten artificial sweeteners, their blood sugar levels spiked upon eating artificial sweeteners, suggesting that the gut bugs were the driving force in the reaction.

The mouse research in particular was “beautifully performed and elegantly done,” said Cathryn Nagler, who researches the connection between gut bugs and food allergies at the University of Chicago and wrote a commentary about the study inNature. The one piece the study was missing, Nagler said, was an explanation for how different gut bug populations might change someone’s ability to process artificial sweeteners.

In trying to understand why certain diseases like food allergies and diabetes have been increasing, Nagler said she looks to things that change gut microbes, such as the introduction of antibiotics, changes in diet, Cesarean-section births, the introduction of formula and the elimination of infectious diseases.

“Now,” she said, “I would add artificial sweeteners to this list.”

Sugar Substitutes Linked to Obesity.

The artificial sweeteners that are widely seen as a way to combat obesity and diabetes could, in part, be contributing to the global epidemic of these conditions.

Sugar substitutes such as saccharin might aggravate these metabolic disorders by acting on bacteria in the human gut, according to a study published by Nature this week (J. Suez et al. Nature; 2014). Smaller studies have previously purported to show an association between the use of artificial sweeteners and the occurrence of metabolic disorders. This is the first work to suggest that sweeteners might be exacerbating metabolic disease, and that this might happen through the gut microbiome, the diverse community of bacteria in the human intestines. “It’s counter-intuitive — no one expected it because it never occurred to them to look,” says Martin Blaser, a microbiologist at New York University.


The findings could cause a headache for the food industry. According to BCC Research, a market-research company in Wellesley, Massachusetts, the market for artificial sweeteners is booming. And regulatory agencies, which track the safety of food additives, including artificial sweeteners, have not flagged such a link to metabolic disorders. In response to the latest findings, Stephen Pagani, a spokesman for the European Food Safety Authority (EFSA) in Parma, Italy, says that, as with all new data, the agency “will decide in due course whether they should be brought to the attention of panel experts for review”.

A team led by Eran Elinav of the Weizmann Institute of Science in Rehovot, Israel, fed mice various sweeteners — saccharin, sucralose and aspartame — and found that after 11 weeks, the animals displayed glucose intolerance, a marker of propensity for metabolic disorders.

To simulate the real-world situation of people with varying risks of these diseases, the team fed some mice a normal diet, and some a high-fat diet, and spiked their water either with glucose alone, or with glucose and one of the sweeteners, saccharin. The mice fed saccharin developed a marked glucose intolerance compared to those fed only glucose. But when the animals were given antibiotics to kill their gut bacteria, glucose intolerance was prevented. And when the researchers transplanted faeces from the glucose-intolerant saccharin-fed mice into the guts of mice bred to have sterile intestines, those mice also became glucose intolerant, indicating that saccharin was causing the microbiome to become unhealthy.

Elinav’s team also used data from an on­going clinical nutrition study that has recruited nearly 400 people in Israel. The researchers noted a correlation between clinical signs of metabolic disorder — such as increasing weight or decreasing efficiency of glucose metabolism — and consumption of artificial sweeteners.

But “this is a bit chicken-and-egg”, says Elinav. “If you are putting on weight, you are more likely to turn to diet food. It doesn’t necessarily mean the diet food caused you to put on weight.”

So his team recruited seven lean and healthy volunteers, who did not normally use artificial sweeteners, for a small prospective study. The recruits consumed the maximum acceptable daily dose of artificial sweeteners for a week. Four became glucose intolerant, and their gut microbiomes shifted towards a balance already known to be associated with susceptibility to metabolic diseases, but the other three seemed to be resistant to saccharin’s effects. “This underlines the importance of personalized nutrition — not everyone is the same,” says Elinav.

He does not yet propose a mechanism for the effect of artificial sweeteners on the micro­biome. But, says Blaser, understanding how these compounds work on some species in the gut might “inspire us in developing new therapeutic approaches to metabolic disease”.

Yolanda Sanz, a nutritionist and vice-chair of the EFSA’s panel on dietetic products, nutrition and allergies, says that it is too soon to draw firm conclusions. Metabolic disorders have many causes, she points out, and the study is very small.

How epigenetic memory is passed through generations: Sperm and eggs transmit memory of gene repression to embryos .

A growing body of evidence suggests that environmental stresses can cause changes in gene expression that are transmitted from parents to their offspring, making ‘epigenetics’ a hot topic. Epigenetic modifications do not affect the DNA sequence of genes, but change how the DNA is packaged and how genes are expressed. Now, scientists have shown how epigenetic memory can be passed across generations and from cell to cell during development.
Images of C. elegans embryos show inheritance and transmission of an epigenetic mark. The 1-cell embryo (left) shows the mark (green) inherited on sperm chromosomes but not on the oocyte chromosomes (pink) from a mutant mother lacking the methylation enzyme PRC2. The 2-cell embryo (right) shows transmission of the mark on the sperm-derived chromosomes in each daughter nucleus.

A growing body of evidence suggests that environmental stresses can cause changes in gene expression that are transmitted from parents to their offspring, making “epigenetics” a hot topic. Epigenetic modifications do not affect the DNA sequence of genes, but change how the DNA is packaged and how genes are expressed. Now, a study by scientists at UC Santa Cruz shows how epigenetic memory can be passed across generations and from cell to cell during development.

The study, published September 19 in Science, focused on one well studied epigenetic modification–the methylation of a DNA packaging protein called histone H3. Methylation of a particular amino acid (lysine 27) in histone H3 is known to turn off or “repress” genes, and this epigenetic mark is found in all multicellular animals, from humans to the tiny roundworm C. elegans that was used in this study.

Ongoing debate

“There has been ongoing debate about whether the methylation mark can be passed on through cell divisions and across generations, and we’ve now shown that it is,” said corresponding author Susan Strome, a professor of molecular, cell and developmental biology at UC Santa Cruz.

Strome’s lab created worms with a mutation that knocks out the enzyme responsible for making the methylation mark, then bred them with normal worms. Using fluorescent labels, they were able to track the fates of marked and unmarked chromosomes under the microscope, from egg cells and sperm to the dividing cells of embryos after fertilization. Embryos from mutant egg cells fertilized by normal sperm had six methylated chromosomes (from the sperm) and six unmarked or “naked” chromosomes (from the egg).

As embryos develop, the cells replicate their chromosomes and divide. The researchers found that when a marked chromosome replicates, the two daughter chromosomes are both marked. But without the enzyme needed for histone methylation, the marks become progressively diluted with each cell division.

“The mark stays on the chromosomes derived from the initial chromosome that had the mark, but there’s not enough mark for both daughter chromosomes to be fully loaded,” Strome said. “So the mark is bright in a one-cell embryo, less bright after the cell divides, dimmer still in a four-cell embryo, and by about 24 to 48 cells we can’t see it anymore.”

The researchers then did the converse experiment, fertilizing normal egg cells with mutant sperm. The methylation enzyme (called PRC2) is normally present in egg cells but not in sperm, which don’t contribute much more than their chromosomes to the embryo. So the embryos in the new experiment still had six naked chromosomes (this time from the sperm) and six marked chromosomes, but now they also had the enzyme.

“Remarkably, when we watch the chromosomes through cell divisions, the marked chromosomes remain marked and stay bright, because the enzyme keeps restoring the mark, but the naked chromosomes stay naked, division after division,” Strome said. “That shows that the pattern of marks that was inherited is being transmitted through multiple cell divisions.”

Important implications

Strome noted that the findings in this study of transmission of histone methylation inC. elegans have important implications in other organisms, even though different organisms use the repressive marker that was studied to regulate different genes during different aspects of development. All animals use the same enzyme to create the same methylation mark as a signal for gene repression, and her colleagues who study epigenetics in mice and humans are excited about the new findings, Strome said.

“Transgenerational epigenetic inheritance is not a solved field–it’s very much in flux,” she said. “There are dozens of potential epigenetic markers. In studies that document parent-to-child epigenetic inheritance, it’s not clear what’s being passed on, and understanding it molecularly is very complicated. We have a specific example of epigenetic memory that is passed on, and we can see it in the microscope. It’s one piece of the puzzle.”

The first author of the Science paper is Laura Gaydos, a graduate student in Strome’s lab at UC Santa Cruz who led the study for her Ph.D. thesis and is now a postdoctoral researcher at Fred Hutchinson Cancer Research Center in Seattle. The other coauthor is Wenchao Wang, who did one of the initial experiments as a graduate student in Strome’s lab several years ago when she was at Indiana University. This research was supported by the National Institutes of Health, a UCSC Dissertation Year Fellowship, and the ARCS Foundation.

Story Source:

The above story is based on materials provided by University of California – Santa Cruz. The original article was written by Tim Stephens. Note: Materials may be edited for content and length.

Journal Reference:

  1. L. J. Gaydos, W. Wang, S. Strome. H3K27me and PRC2 transmit a memory of repression across generations and during development. Science, 2014; 345 (6203): 1515 DOI: 10.1126/science.1255023

Artificial Sweeteners May Contribute to Metabolic Disorders .

Artificial sweeteners are a roughly $1.5 billion industry worldwide, often marketed as helpful for managing obesity and diabetes.

But some new research suggests sugar substitutes could actually contribute to soaring rates of obesity and diabetes by spurring metabolic changes linked to those diseases.

artificial sweetener packets

As Alison Abbott reports this week in Nature, a research team in Israel examined both mice and people for metabolic responses to consuming artificial sweeteners. Groups of mice consumed diets for 11 weeks that either included an artificial sweetener -– saccharin, sucralose or aspartame – or a natural sugar: glucose or sucrose. The mice consuming the artificial sweeteners became glucose intolerant: a metabolic disorder in which the body has difficulty digesting the sugar glucose (a carbohydrate), resulting in overly high blood sugar levels. Glucose intolerance is linked to diabetes, and is sometimes a factor in rising body weight.

Saccharin had the most impact on glucose tolerance. Other factors, such as whether the mice were already lean or obese, how much they ate and drank, or how much exercise they got, did not change the results.

The team then fed mice with diets containing either natural sugar or saccharin. They found that the saccharin-consuming mice developed glucose intolerance and that their types of gut bacteria changed. The mice consuming glucose or sucrose did not show these effects.

When the saccharin-consuming mice were fed antibiotics, their glucose intolerance stopped. When gut bacteria from saccharin-exposed mice were transplanted into mice with sterile guts, these mice developed glucose intolerance.

Taken as a whole, these findings suggest that the sugar substitutes were affecting the gut bacteria, which in turn caused the glucose intolerance.

To begin determining if humans would be prone to the same reactions, the researchers examined data from 400 human subjects in one Israeli clinical nutrition study. They found a correlation between consumption of artificial sweeteners and weight gain or glucose intolerance. But this didn’t necessarily indicate a link, because people in the study might have started consuming artificial sweeteners in response to gaining weight, rather than gaining weight because they consumed the sugar substitutes.

So the scientists also “recruited seven lean and healthy volunteers, who did not normally use artificial sweeteners, for a small prospective study,” writes Abbott. “The recruits consumed the maximum acceptable daily dose of artificial sweeteners for a week. Four became glucose intolerant, and their gut microbiomes shifted towards a balance already known to be associated with susceptibility to metabolic diseases, but the other three seemed to be resistant to saccharin’s effects.”

When the gut bacteria of the affected human subjects were transplanted into sterile-gut mice, the mice developed glucose intolerance. Mice receiving a bacteria transplant from the saccharin-resistant human participants did not.

So far this study is most informative in terms of how sugar substitutes affect mice. As this write-up by the U.K.’s National Health Service notes, more thorough human testing is needed to prove that they’re more dangeous than helpful for people. But if the findings move you to action, one option is to curb or cut both the natural and artificial sweeteners in your diet.

Fluoroquinolone bested other antibiotics in Haemophilus influenzae-related pneumonia.

For adults with Haemophilus influenzae-related community acquired pneumonia, fluoroquinolones were significantly associated with early clinical response rates that were better than those seen with other antibiotics, based on the findings of a German study.

“Initial treatment with any fluoroquinolone was the only positive predictor of early clinical response, and use of macrolide monotherapy was the only negative predictor of early clinical response,” Dr. Christina Forstner, a researcher at the Medical University of Vienna in Austria, said at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

Courtesy Dr. W.A. Clark/CDC

Initial treatment with any fluoroquinolone was the only positive predictor of early clinical response, Dr. Forstner said.

The multi-center, observational, prospective, cohort study was conducted between 2002 and 2012 in 171 adults who had community acquired pneumonia and tested positive forH.influenzae. In 124 patients, H.influenzae was the sole pathogen detected, whereas 47 patients had at least one other co-infection.

The primary end point of the study was an early clinical response ‑ clinical stability by day 4 of treatment. The secondary end point was clinical cure anywhere at day 14. The choice of antimicrobial treatment was left to the discretion of individual clinicians.

Early clinical response rates were seen for 46 of 47 patients (97.6%) given any fluoroquinolone, with 100% clinical cure by day 14. Fluoroquinolone monotherapy achieved a nearly 100% early clinical response rate (39 out of 40 patients), and complete clinical cure was seen in all patients by day 14. The rates were significantly different from those seen with other antibiotics (P = .01).

An early clinical response rate was seen in 92 of 108 patients (85.2%) given any beta-lactam. Beta-lactam monotherapy achieved an early clinical response rate in 63 out of 74 cases, with a clinical cure rate at day 14 in 68 out of 74 cases.

An early clinical response rate was seen in 29 of 36 patients (80.6%) who received any macrolide; an early clinical response rate was seen in 8 of 12 patients given monotherapy with a macrolide. Clinical cure rate at day 14 was 32 out of 36 patients given any macrolide, and 11 out of 12 given macrolide monotherapy.

The median duration of therapy was, according to Dr. Forstner, “quite long” at 10 days. Monotherapy was used in 78.4% of patients, and oral treatments in 63.7%.

The overall early clinical response rate was 88%, with an overall clinical cure of 93% on day 14, and of 95.9% on day 28.

A univariate analysis of age, body mass index, severity of disease, co-infection, and treatments used indicated the only factor associated with an early clinical response was the use of any fluoroquinolone (odds ration, 8.8). Macrolide monotherapy was associated with a negative clinical response (OR, 0.239).

97% of Terminal Cancer Patients Previously Had This Dental Procedure

Do you have a chronic degenerative disease? If so, have you been told, “It’s all in your head?” Well, that might not be that far from the truth…

The root cause of your illness may be in your mouth.


There is a common dental procedure that nearly every dentist will tell you is completely safe, despite the fact that scientists have been warning of its dangers for more than 100 years. Every day in the United States alone, 41,000 of these dental procedures are performed on patients who believe they are safely and permanently fixing their problem.

What is this dental procedure?

The root canal.

More than 25 million root canals are performed every year in this country.

Root-canaled teeth are essentially “dead” teeth that can become silent incubators for highly toxic anaerobic bacteria that can, under certain conditions, make their way into your bloodstream to cause a number of serious medical conditions—many not appearing until decades later.

Most of these toxic teeth feel and look fine for many years, which make their role in systemic disease even harder to trace back.

Sadly, the vast majority of dentists are oblivious to the serious potential health risks they are exposing their patients to, risks that persist for the rest of their patients’ lives. The American Dental Association claims root canals have been proven safe, but they have NO published data or actual research to substantiate this claim.

Fortunately, I had some early mentors like Dr. Tom Stone and Dr. Douglas Cook, who educated me on this issue nearly 20 years ago. Were it not for a brilliant pioneering dentist who, more than a century ago, made the connection between root-canaled teeth and disease, this underlying cause of disease may have remained hidden to this day. The dentist’s name was Weston Price—regarded by many as the greatest dentist of all time.

Weston A. Price: World’s Greatest Dentist

Most dentists would be doing an enormous service to public health if they familiarized themselves with the work of Dr. Weston Pricei. Unfortunately, his work continues to be discounted and suppressed by medical and dental professionals alike.

Dr. Price was a dentist and researcher who traveled the world to study the teeth, bones, and diets of native populations living without the “benefit” of modern food. Around the year 1900, Price had been treating persistent root canal infections and became suspicious that root-canaled teeth always remained infected, in spite of treatments. Then one day, he recommended to a woman, wheelchair bound for six years, to have her root canal tooth extracted, even though it appeared to be fine.

She agreed, so he extracted her tooth and then implanted it under the skin of a rabbit. The rabbit amazingly developed the same crippling arthritis as the woman and died from the infection 10 days later. But the woman, now free of the toxic tooth, immediately recovered from her arthritis and could now walk without even the assistance of a cane.

Price discovered that it’s mechanically impossible to sterilize a root-canaled (e.g. root-filled) tooth.

He then went on to show that many chronic degenerative diseases originate from root-filled teeth—the most frequent being heart and circulatory diseases. He actually found 16 different causative bacterial agents for these conditions. But there were also strong correlations between root-filled teeth and diseases of the joints, brain and nervous system. Dr. Price went on to write two groundbreaking books in 1922 detailing his research into the link between dental pathology and chronic illness. Unfortunately, his work was deliberately buried for 70 years, until finally one endodontist named George Meinig recognized the importance of Price’s work and sought to expose the truth.

Dr. Meinig Advances the Work of Dr. Price

Dr. Meinig, a native of Chicago, was a captain in the U.S. Army during World War II before moving to Hollywood to become a dentist for the stars. He eventually became one of the founding members of the American Association of Endodontists (root canal specialists).

In the 1990s, he spent 18 months immersed in Dr. Price’s research. In June of 1993, Dr. Meinig published the book Root Canal Cover-Up, which continues to be the most comprehensive reference on this topic today. You can order your copy directly from the Price-Pottenger Foundationii.

What Dentists Don’t Know About the Anatomy of Your Teeth

Your teeth are made of the hardest substances in your body.

In the middle of each tooth is the pulp chamber, a soft living inner structure that houses blood vessels and nerves. Surrounding the pulp chamber is the dentin, which is made of living cells that secrete a hard mineral substance. The outermost and hardest layer of your tooth is the white enamel, which encases the dentin.

The roots of each tooth descend into your jawbone and are held in place by the periodontal ligament. In dental school, dentists are taught that each tooth has one to four major canals. However, there are accessory canals that are never mentioned. Literally miles of them!

Just as your body has large blood vessels that branch down into very small capillaries, each of your teeth has a maze of very tiny tubules that, if stretched out, would extend for three miles. Weston Price identified as many as 75 separate accessory canals in a single central incisor (front tooth). For a more detailed explanation, refer to an article by Hal Huggins, DDS, MS, on the Weston A. Price Foundation website.iii (These images are borrowed from the Huggins article.)

Microscopic organisms regularly move in and around these tubules, like gophers in underground tunnels.

When a dentist performs a root canal, he or she hollows out the tooth, then fills the hollow chamber with a substance (called guttapercha), which cuts off the tooth from its blood supply, so fluid can no longer circulate through the tooth. But the maze of tiny tubules remains. And bacteria, cut off from their food supply, hide out in these tunnels where they are remarkably safe from antibiotics and your own body’s immune defenses.

The Root Cause of Much Disease

Under the stresses of oxygen and nutrient deprivation, these formerly friendly organisms morph into stronger, more virulent anaerobes that produce a variety of potent toxins. What were once ordinary, friendly oral bacteria mutate into highly toxic pathogens lurking in the tubules of the dead tooth, just awaiting an opportunity to spread.

No amount of sterilization has been found effective in reaching these tubules—and just about every single root-canaled tooth has been found colonized by these bacteria, especially around the apex and in the periodontal ligament. Oftentimes, the infection extends down into the jawbone where it creates cavitations—areas of necrotic tissue in the jawbone itself.

Cavitations are areas of unhealed bone, often accompanied by pockets of infected tissue and gangrene. Sometimes they form after a tooth extraction (such as a wisdom tooth extraction), but they can also follow a root canal. According to Weston Price Foundation, in the records of 5,000 surgical cavitation cleanings, only two were found healed.

And all of this occurs with few, if any, accompanying symptoms. So you may have an abscessed dead tooth and not know it. This focal infection in the immediate area of the root-canaled tooth is bad enough, but the damage doesn’t stop there.

Root Canals Can Lead to Heart, Kidney, Bone, and Brain Disease

As long as your immune system remains strong, any bacteria that stray away from the infected tooth are captured and destroyed. But once your immune system is weakened by something like an accident or illness or other trauma, your immune system may be unable to keep the infection in check.

These bacteria can migrate out into surrounding tissues by hitching a ride into your blood stream, where they are transported to new locations to set up camp. The new location can be any organ or gland or tissue.

Dr. Price was able to transfer diseases harbored by humans to rabbits, by implanting fragments of root-canaled teeth, as mentioned above. He found that root canal fragments from a person who had suffered a heart attack, when implanted into a rabbit, would cause a heart attack in the rabbit within a few weeks.

He discovered he could transfer heart disease to the rabbit 100 percent of the time! Other diseases were more than 80 percent transferable by this method. Nearly every chronic degenerative disease has been linked with root canals, including:

-Heart disease
-Kidney disease
-Arthritis, joint, and rheumatic diseases
-Neurological diseases (including ALS and MS)
-Autoimmune diseases (Lupus and more)

There may also be a cancer connection. Dr. Robert Jones, a researcher of therelationship between root canals and breast cancer, found an extremely high correlation between root canals and breast cancer.iv He claims to have found the following correlations in a five-year study of 300 breast cancer cases:

-93 percent of women with breast cancer had root canals
-7 percent had other oral pathology
-Tumors, in the majority of cases, occurred on the same side of the body as the root canal(s) or other oral pathology

Dr. Jones claims that toxins from the bacteria in an infected tooth or jawbone are able to inhibit the proteins that suppress tumor development. A German physician reported similar findings. Dr. Josef Issels reported that, in his 40 years of treating “terminal” cancer patients, 97 percent of his cancer patients had root canals. If these physicians are correct, the cure for cancer may be as simple as having a tooth pulled, then rebuilding your immune system.

Good Bugs Gone Bad

How are these mutant oral bacteria connected with heart disease or arthritis? The ADA and the AAE claim it’s a “myth” that the bacteria found in and around root-canaled teeth can cause diseasev. But they base that on the misguided assumption that the bacteria in these diseased teeth are the SAME as normal bacteria in your mouth—and that’s clearly not the case.

Today, bacteria can be identified using DNA analysis, whether they’re dead or alive, from their telltale DNA signatures.

In a continuation of Dr. Price’s work, the Toxic Element Research Foundation (TERF) used DNA analysis to examine root-canaled teeth, and they found bacterial contamination in 100 percent of the samples tested. They identified 42 different species of anaerobic bacteria in 43 root canal samples. In cavitations, 67 different bacteria were identified among the 85 samples tested, with individual samples housing between 19 to 53 types of bacteria each. The bacteria they found included the following types:


Are these just benign, ordinary mouth bugs? Absolutely not. Four can affect your heart, three can affect your nerves, two can affect your kidneys, two can affect your brain, and one can infect your sinus cavities… so they are anything BUT friendly! (If you want see just how unfriendly they can be, I invite you to investigate the footnotes.)

Approximately 400 percent more bacteria were found in the blood surrounding the root canal tooth than were found in the tooth itself, suggesting the tooth is the incubatorand the periodontal ligament is the food supply. The bone surrounding root-canaled teeth was found even HIGHER in bacterial count… not surprising, since bone is virtual buffet of bacterial nutrients.

Since When is Leaving A Dead Body Part IN Your Body a Good Idea?

There is no other medical procedure that involves allowing a dead body part to remain in your body. When your appendix dies, it’s removed. If you get frostbite or gangrene on a finger or toe, it is amputated. If a baby dies in utero, the body typically initiates a miscarriage.

Your immune system doesn’t care for dead substances, and just the presence of dead tissue can cause your system to launch an attack, which is another reason to avoid root canals—they leave behind a dead tooth.

Infection, plus the autoimmune rejection reaction, causes more bacteria to collect around the dead tissue. In the case of a root canal, bacteria are given the opportunity to flush into your blood stream every time you bite down.

Why Dentists Cling to the Belief Root Canals are Safe

The ADA rejects Dr. Price’s evidence, claiming root canals are safe, yet they offer no published data or actual research to substantiate their claim. American Heart Association recommends a dose of antibiotics before many routine dental procedures to prevent infective endocarditis (IE) if you have certain heart conditions that predispose you to this type of infection.

So, on the one hand, the ADA acknowledges oral bacteria can make their way from your mouth to your heart and cause a life-threatening infection.

But at the same time, the industry vehemently denies any possibility that these same bacteria—toxic strains KNOWN to be pathogenic to humans—can hide out in your dead root-canaled tooth to be released into your blood stream every time you chew, where they can damage your health in a multitude of ways.

Is this really that large of a leap? Could there be another reason so many dentists, as well as the ADA and the AAE, refuse to admit root canals are dangerous? Well, yes, as a matter of fact, there is. Root canals are the most profitable procedure in dentistry.

What You Need to Know to AVOID a Root Canal

I strongly recommend never getting a root canal. Risking your health to preserve a tooth simply doesn’t make sense. Unfortunately, there are many people who’ve already have one. If you have, you should seriously consider having the tooth removed, even if it looks and feels fine. Remember, as soon as your immune system is compromised, your risk of of developing a serious medical problem increases—and assaults on your immune system are far too frequent in today’s world.

If you have a tooth removed, there are a few options available to you.

1)Partial denture: This is a removable denture, often just called a “partial.” It’s the simplest and least expensive option.
2)Bridge: This is a more permanent fixture resembling a real tooth but is a bit more involved and expensive to build.
3)Implant: This is a permanent artificial tooth, typically titanium, implanted in your gums and jaw. There are some problems with these due to reactions to the metals used. Zirconium is a newer implant material that shows promise for fewer complications.

But just pulling the tooth and inserting some sort of artificial replacement isn’t enough.

Dentists are taught to remove the tooth but leave your periodontal ligament. But as you now know, this ligament can serve as a breeding ground for deadly bacteria. Most experts who’ve studied this recommend removing the ligament, along with one millimeter of the bony socket, in order to drastically reduce your risk of developing an infection from the bacterially infected tissues left behind.

I strongly recommend consulting a biological dentist because they are uniquely trained to do these extractions properly and safely, as well as being adept at removing mercury fillings, if necessary. Their approach to dental care is far more holistic and considers the impact on your entire body—not JUST your mouth.

If you need to find a biological dentist in your area, I recommend visiting, a resource sponsored by Consumers for Dental Choice. This organization, championed by Charlie Brown, is a highly reputable organization that has fought to protect and educate consumers so that they can make better-informed decisions about their dental care. The organization also heads up the Campaign for Mercury-Free Dentistry.

Topiramate may have benefit as a weight-loss drug .

The drug topiramate can help people lose weight as long as they can tolerate the side effects, according to authors of a new study that reviewed the medical literature, according to Brazilian researchers.

The drug topiramate can help people lose weight as long as they can tolerate the side effects, according to authors of a new study that reviewed the medical literature.

Brazilian researchers are presenting the results at The Endocrine Society’s 93rd Annual Meeting in Boston.

Among more than 3,300 overweight or obese patients, those who took topiramate for at least four months lost 11.8 pounds more on average than individuals who took “dummy” pills, or placebo, found the meta-analysis, a systematic and quantitative review of published studies.

“Topiramate is not an approved drug for the treatment of obesity. Data from individual clinical trials might not be sufficient to support physicians’ decision to prescribe it for this use, and robust evidence of its safety is lacking,” said lead investigator Caroline Kramer, MD, PhD. She is an endocrinologist at Clinic Hospital of Porto Alegre in Brazil.

Currently topiramate is approved as an anti-convulsant for treatment of seizure disorders and for prevention in adults of migraine headaches.

The investigators pooled the research results of 10 randomized, controlled clinical trials (considered the gold standard in scientific research) that evaluated the benefits and adverse effects of topiramate prescribed for weight loss. They analyzed data about the effectiveness of topiramate on weight loss in 3,320 patients and data on adverse effects in 6,620 patients, she said.

According to the analysis, the duration and dosage of treatment affected the weight-loss benefits. Weight loss was higher when the drug was prescribed at doses of 96 to 200 milligrams per day for more than 28 weeks compared with less than 28 weeks, the authors reported. Compared with study subjects who took the placebo, topiramate-treated patients were seven times likelier to lose more than 10 percent of their body weight.

However, the authors found that patients were nearly two times more likely to stop topiramate treatment because of side effects than were those receiving placebo. The most common side effects, according to Kramer, included a burning sensation (paresthesia), typically around the mouth; impaired taste; and psychomotor disturbances, including slower thinking and reduced physical movements. Difficulty concentrating and memory impairment also were increased.

“Topiramate has a substantial effect on weight loss, at least comparable to the weight loss that other anti-obesity drugs induce,” Kramer said. “We have so few pharmacological options for the treatment of obesity that I believe topiramate can be a useful tool together with diet and exercise.”

She said it is important, however, for patients to understand the drug’s known possible side effects and to be aware that it may have uncommon side effects that researchers have not yet observed.

The National Institutes of Health caution that people should use prescription weight-loss medications only if they are at increased risk of health problems because of their excess weight.