Gram Negative Bacteria and Obesity – 180 Degree Health

By Andrew Kim 

Introduction

As the research evolves, the matter of diet and nutrition is being forced to be recognized as not only the most poorly understood of all the sciences but also one of the most complex, outranking all the others.

Weight loss is a recurrent theme on this site and this should be expected, as obesity is the most common “disease” in the United States.1 But herein lies a wrinkle that adds to the complexity of this matter: What constitutes a healthy weight is not an objective, uniformly agreed upon standard.

Suffice it to say here, we know that having excess body fat is strongly linked to cardiovascular disease, kidney disease, diabetes, and hypertension.  It also aggravates arthritis, gout, gallbladder disease, and blood lipid disorders.  And, it appears to aggravate certain cancers.2 

The interplay among the fat tissue, organs, muscles, and immune system is, to me, highly complex – even after drawing out all the ways in which they do in great detail.  However, up until doing researching for this post, I hadn’t fully appreciated the dimension added to this interplay by the intestinal flora and biome.

In light of the extreme claims made on behalf of (expensive) probiotic and prebiotic supplements, such as in the video below…

…my inaugural post for this site will present, in my estimation, the most important experiments that have added clarity about the connection among intestinal flora, metabolism, and weight loss.  What will be clear is that:

  1. There are observed differences between the intestinal flora of lean and the intestinal flora of obese individuals.
  2.   The interaction between the host and the intestinal flora is intricate and entails changes in the host gene expression involved in nutrient – particularly carbohydrate – processing and appetite regulation, which are not fully understood.
  3.   High-fat diets promote the passage of a bacterial poison called endotoxin into the body, potentially leading to endotoxemia (arbitrarily defined as when endotoxin levels rise by 2- to 3-fold above normal levels).
  4.  Weight loss is probably the great equalizer in that weight loss, in and of itself, reverts the intestinal flora and biome of obese individuals to that of lean individuals.

OBESITY AND THE INTESTINAL FLORA

Obesity changes the gut flora, and these changes have been directly correlated with a host of metabolic imbalances and diseases in animals.  This fact should not be a surprise anymore, as the intestinal flora is now known to play an indispensable role in the nutrient metabolism – particularly carbohydrate metabolism – of its host.  It was shown, for instance, that in the rectum, over 100 genes are regulated differentially by intestinal flora; and in the jejunum, over 200 genes.3

But test tube studies like the one described above are obviously limited in what we can take away from them.  Luckily, many of the assumptions and hypotheses about the intestinal flora are testable in living organisms.

In one now classic experiment, despite eating 30 percent less food than germ-free mice, normal mice were 40 percent fatter than germ-free mice.  In a follow up experiment, upon inoculating germ-free mice with the flora from normal mice, the germ-free mice became about 60 percent fatter and developed insulin resistance after 2 weeks, despite eating less food than normal.4 Leptin levels increased, too, and though the authors merely correlated the increase in leptin to the increase in fatness, it was probably also driving the insulin resistance that had developed.

Since living in a germ-free environment isn’t possible and since wiping out the flora in our intestines entirely would lead to serious deficiencies and malnutrition, we could, next, investigate dietary interventions that alter the microbial biome in a way that matches that of healthy and lean individuals.

Generally, mice fed on high-fat diets have a significant increase in endotoxin levels – indicating either a greater ratio of gram-negative bacteria to gram-positive bacteria in the intestines, as only gram-negative bacteria have coats that bear endotoxin.  Endotoxin is quite toxic to the human body5 and large exposures to it can be quickly life threatening and fatal.

In short, endotoxin creates a state of shock in the human body – known as septic shock.  Lucky for us, to get to this point, very large bacterial invasions into the body are needed by way of breaks in the skin – including the “skin” of the intestines.

However, at relatively lower, chronic doses, endotoxin:

  • Favors wide spread blood clotting
  • Leads to fatty liver conditions
  • Promotes oxidative stress and metabolic disorders (including glucose intolerance and insulin resistance)
  • Initiates an immune response (however, I’m open to the possibility that this effect, though the mechanisms are less clear to me, may actually serve the host favorably in the big picture)5

Further, mice fed on high-fat diets, compared to high-carbohydrate diets, have reduced concentrations of Bifidobacterium species – a major type of gram-positive bacteria normally present in the intestines of mammals.  A lower concentration of Bifidobacterium species creates a vacuum in which more virulent, endotoxin-bearing gram-negative bacteria could seed and proliferate. (Because of the presence of endotoxin in their coats, gram-negative bacteria are not only more virulent than gram-positive bacteria, but they are also more resistant to antibiotics, as antibiotics have difficulty penetrating this outer coat.)  In fact, Bifidobacterium species reduce the intestinal endotoxin load, and at the same time, strengthens the intestinal barrier.6

I mention this fact to point out how a simple dietary change could, by altering the intestinal biome, bring about marked changes in a person’s metabolism and health – regardless of the amount of calories consumed.

Further, the introduction of Bifidobacterium species has been shown to reduce the intestinal endotoxin load, improve the barrier functioning of the intestinal wall, and protect against obesity and endotoxemia brought about by a high-fat diet.7

Although the majority of studies showing an increase an endotoxin levels caused by high-fat diets were performed in rodents, I think, considering the major way in which endotoxin moves into the body, it’s reasonable to assume that the same result would be seen in humans.

Endotoxin is continuously generated and released into the intestines by bacteria upon their destruction or death.  From there, endotoxin is transported into the capillaries, which surround the intestines, via newly made lipoproteins called chylomicrons, whose formation is stimulated by the presence of dietary fat.  So following a high-fat meal, a rise, albeit a usually modest rise, of endotoxin would be seen in the blood.

Before I leave this train of thought and move cautiously along to my recommendations, we need to consider one additional seminal experiment, which was carried out in humans.  In said experiment, weight loss – via a low-fat diet or a calorie restricted low-carbohydrate diet – resulted in a shift in the intestinal microbial ecology in obese subjects, more closely matching that of lean controls.4 In other words, weight loss, in and of itself, altered the intestinal microbial biome favorably.

RECOMMENDATIONS

I’ve always been skeptical about the use of probiotics and prebiotics, and up until doing research for this post saw little evidence to justify their use for any condition – the evidence was so thin.

However, evidence from clinical trials in humans is emerging on the use of prebiotics and probiotics – particularly for the reduction in heart disease risk.

But whether an altered intestinal biome through the use of probiotics or prebiotics could accelerate fat lass and eradicate obesity in humans is unclear to me at this point and I seriously have my doubts about the effectiveness of orally administered probiotic and prebiotic supplements and foods.

From my own experiments and observations, I have been an advocate for, foremost, maximizing and expanding the capacity of oxidative energy generation to promote weight loss and health at the same time – cliché as this is. (At least until fecal probiotic transplants are properly tested for safely reducing body fat and become easily available to us all).  Fundamentally, this entails the following:

  • Increasing oxygen delivery to cells.
  • Supplying adequate amounts of B vitamins, as many of the coenzymes and carrier molecules that operate (as cardinal adsorbents) in the mitochondrial respiratory chain are made from thiamine, riboflavin, niacin, etc.  Ubiquinone, also known as CoQ10, is also important, and the more cholesterol we produce, the more ubiquinone will be made in the amounts needed by cells. Sucrose, namely its fructose half, is a potent stimulator of cholesterol synthesis.8
  • Maintaining the optimal rate of secretion, blood levels, and conversion of thyroid hormone, as thyroid hormone is the main regulator of a person’s metabolic rate and stimulates all reactions in the mitochondria involved in oxidative metabolism.

Regarding the first point, suffice it to say here, putting a brake on the excessive release and oxidation of fatty acids enhances the delivery of oxygen to cells and prevents tissue hypoxia.  Ditching high-fat low-carbohydrate diets serve this purpose.  In addition, “fast-moving” blood is essential, so platelet aggregation and fibrin production must be kept under control.

Because absorbed endotoxin stimulates fibrin production (and interferes with oxidative metabolism), its entry into the body must be minimized (or its removal from the body must be cranked up).

Vitamins K1 and K2, for instance, by enhancing the activity of an intestinal enzyme, minimizes the errant passage of endotoxin (and other harmful substances) into the body.  Vitamin K can be gotten from green vegetables and smaller amounts from fermented dairy and soy products.

Salicylates block the production of a certain prostaglandin that causes platelets to clump and blood vessels to constrict.  Aspirin and other non-steroidal antiinflammatory drugs (NSAIDs) are end products of salicylates, which occur abundantly in plants – especially in fruits.  Gotten from plants – namely fruits – salicylates are delivered to the body at a safer rate and concentration than drugs.  Salicylates also happen to prevent some of the inflammatory responses initiated by endotoxin.

Stress should be kept as low as possible.  Space does not permit me to go further into what I mean here except to say that cravings – namely for salt, sugar, and more food – should not be ignored or suppressed.  This act of defiance imposes undue stress on the body, further enhancing fibrin production.  Listen closely to your body, not diet gurus or Jenny Craig, please.

Of obvious note yet still worth bringing to your attention, one should avoid smoking and excessive alcohol consumption to promote efficient oxidative metabolism because smoking increases the exposure to carbon monoxide, a metabolic poison, and alcohol increases the permeability of the intestinal barrier.

And finally, although the research and evidence for this last recommendation is relatively scant, I would try to eat smaller meals spaced equally throughout the day, instead of large, infrequent meals.  Compared to large meals, I think small meals place less burden on the liver, keep blood sugar levels more steady, reduce endotoxin levels, and decrease the likelihood of storing the food you eat as fat, rather than to generate energy.

Andrew KimAndrew Kim is a graduate of the University of Maryland with degrees in Microbiology and Japanese. His blog has garnered much attention since its release earlier this year. Read more of Kim’s work at www.andrewkimblog.com

 REFERENCES

  1. Overweight and Obesity. Centers for Disease Control and Prevention (2013). at http://www.cdc.gov/obesity/data/adult.html
  2. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults–The Evidence Report. National Institutes of Health. Obesity research 6 Suppl 2, 51S–209S (1998).
  3. Mutch, D. M. et al. Impact of commensal microbiota on murine gastrointestinal tract gene ontologies. Physiological genomics 19, 22–31 (2004).
  4. Ley, R. E. et al. Obesity alters gut microbial ecology. Proceedings of the National Academy of Sciences of the United States of America 102, 11070–5 (2005).
  5. Rang, H. P., Dale, M. M., Ritter, J. M., Flower, R. J. Henderson, G. Rang Dale’s Pharmacology. 792 (2011).
  6. Griffiths, E. A. et al. In vivo effects of bifidobacteria and lactoferrin on gut endotoxin concentration and mucosal immunity in Balb/c mice. Digestive diseases and sciences 49, 579–89 (2004).
  7. Cani, P. D. et al. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia 50, 2374–83 (2007).
  8. Silbernagel, G. et al. Cholesterol synthesis is associated with hepatic lipid content and dependent on fructose/glucose intake in healthy humans. Experimental diabetes research 2012, 361863 (2012).

Examining the link between bacteria and obesity

We have, it seems, moved on from acknowledging it takes a village to raise a human being. We are well into the realm of realization that it takes a village just to be one. More and more studies are demonstrating the importance of the germs that outnumber our cells by an order of magnitude at least, to virtually every aspect of physiology. But while epiphanies of this sort are redolent with promise, they can be dizzying as well, and pose a threat of disequilibrium and distraction. If we can miss the forest for the trees, there is, I think, a comparable risk of missing the importance of lifestyle for the Lactobacilli. My motivation here is the hope that we will not.

While I can no longer readily recall what life was like before email, I certainly do recall medical practice before the widespread popularity of probiotics. Only very recently did the use of ingestible bacteria transition from the realm of far-fetched to all-but-standard, and from “you must be kidding!” to “where to do I get mine?” Not all that long ago, the only good germ was a dead germ.

Progress since the initial uptake of the probiotic concept has been astounding. The now well-established potential to prevent and treat C. difficile colitis, a dire complication of antibiotic therapy, with probiotics is a considerable advance all by itself.

The more we’ve learned about the importance of our resident microbes, the more we’ve learned about the need and opportunity to learn more. The process may be likened to climbing a hill, and then gaining a view of the higher hills and mountains beyond. There is a lot of climbing left to do.

One peak now within view involves the important relationships among our immune system, cohabiting bacteria, and other organisms. In An Epidemic of Absence, Moises Velaszquez-Manoff makes a thorough and compelling case for the unintended consequences of sanitizing our environments and the eradication of parasites. How best to apply such lessons to the management of allergy and autoimmune disease is a work in progress, but that it’s vitally important work now seems abundantly clear.

The other peak before us is the one that worries me a bit. It beckons with tantalizing new findings related to weight control.

We have known for quite some time that commensal microbes play a vital role in digestion. In fact, we surmised this about bacteria living in our guts before we knew much else about them; after all, what else would they be doing there? More recently, we have come to learn that bacterial colony counts influence our energy efficiency and the number of calories we can extract from food. Differences in the microbiome can make it harder or easier to lose weight, and may account for more flagrant cases of weight loss resistance. In some instances, when all else fails, the wholesale transplantation of gut microbes may allow for weight control.

This provocative tale is further embellished by a cluster of recent papers in preeminent scientific journals. An article published in Nature Reviews in early August explores the causal pathway from intestinal microbes to obesity risk. A study published in late August in Nature compared the microbiota in 123 lean and 169 obese Danish adults. The authors report greater genetic variety among gut microbes in lean individuals than obese. A brief report of an intervention in the same issue of the journal reported an increase in the genetic richness of gut microbes when obese and overweight individuals were put on a weight-reducing diet. And even more of Nature’s rarefied real estate has been allocated to this topic to accommodate commentaries and editorials.

And a report in Science indicated that the gut microbes from obese adult twins could make germ-free mice get fat, while the gut microbes from their lean siblings had the opposite effect.

Why does this all worry me?

I fully acknowledge the almost certain importance of our microbial diversity to energy balance and weight regulation. I accept that indelible links are being forged among genes, germs, and resultant girth.

But we are all too easily distracted from the accessible means of both losing weight and finding health, by new and exotic theories. Excessive preoccupation with the microbiome could lead us into our next great boondoggle.

Consider that behaviors we control directly, as opposed to microbial colonies we may not, explain 80 percent of the variation in the risk for all major chronic diseases. Consider that overwhelmingly, when people eat well and exercise, they lose weight — and if the behaviors persist, so does the weight loss. Consider that obesity was rather uncommon a half century ago in the days before drive-through fast-food restaurants, a vast proliferation of junk foods, and a comparable proliferation of labor-saving technologies.

In other words, while scrutiny of our microbes may help account for enigmatic cases of weight gain, they are, for most of us, the trees that may cause us to overlook the forest. The fixable causes of obesity and chronic disease are on prominent display, all around us. Most of us will gain weight when we take in too many calories, even if from wholesome sources. Most of us will lose weight if we restrict calories enough, even if those calories come from Twinkies. Energy balance does not seem to require a bacterial referendum.

For the most part, people who exercise diligently and eat very well are both leaner and healthier than others who don’t. What a remarkable coincidence it would be if those who best attended to calories in and calories out just happened to be those with the genes and germs conducive to trim guts.

This does not mean the germs and genes in our guts are not germane to weight and health; they clearly are. But the available evidence suggests they are at least as much effects as causes.

In other words, the same adverse exposures that tend to make us sick and fat appear to do much the same to our resident bugs. It doesn’t much change the relevance of junky diets and physical inactivity to poor health and weight gain to note that along with all of the other adverse effects of such behaviors, they disrupt and distort the microbiome. All this really means as that we, and our germs, are in this together — we flourish, or founder, together.

For a quick analogy, imagine if we had just discovered atherosclerosis and reached the conclusion that it is the “real” cause of heart disease. That would be true, but it would be a serious mistake to toss out what we knew about tobacco, physical activity, and diet as a result. Those factors influence atherosclerosis, which in turn influences the likelihood of heart attack. Similarly, shifts in our bacterial colonies may be part of the pathway by which behaviors translate into changes in both weight, and health. This is in no way an invitation to jettison anything we already knew about the importance of those behaviors.

There may well be some opportunities to address the microbiome directly, from probiotics to fecal transplant. There are, analogously, ways to address atherosclerotic plaque directly with angioplasty and coronary bypass surgery. But just as lifestyle can keep arteries healthy in the first place, or even restore them to health, so too, it seems, can the very same lifestyle practices that protect our health do the same for our inner menagerie.

Over the years, we have heard about many “obesity genes.” But these genes were around long before obesity was a salient public health concern. Genes that haven’t changed recently can’t really account for recent changes in epidemiology. Similarly, while our understanding of our intimate codependence on gut microbes is fairly recent, the codependence is not. The bugs were there all along. If they have suddenly become complicit in epidemic obesity, it might be tempting to pass the buck to the bugs, but it begs the question: What changed them?

This, in turn, offers the silver lining of insight within the dark clouds of potential diversion. One of the prevailing mistakes about obesity is to pin it all on personal responsibility. There is, clearly, a case for personal responsibility; but the choices we make are in turn governed by the choices we have. It never made sense to presume that the current generation of 7-year-olds was less endowed with personal responsibility than every prior generation of 7-year-olds; but they sure are fatter! It makes even less sense to ascribe less personal responsibility to the current generation of Saccharomyces.

Of course, the “fault” lies not in our Saccharomyces! The explanations for what is awry within us are all around us; the very factors of lifestyle, environment and culture that have changed us have changed our resident flora as well. The behaviors that lead to better health and healthier weight may do so in part by moderating the expression of genes, and favorably shifting the populations of gut microbes.

It takes a healthy village within, it seems, to be a healthy human being. It still takes healthy choices by that human being to tend the village.

David L. Katz is the founding director, Yale-Griffin Prevention Research Center. He is the author of Disease-Proof: The Remarkable Truth About What Makes Us Well.

Healthy gut bacteria prevent obesity: Study




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(NaturalNews) The key to shedding those excess pounds and achieving that lean figure you have always dreamed about could be as simple as eating more bacteria. A new study out of Washington University in St. Louis has found that maintaining healthy and balanced gut bacteria — that is, the beneficial microbes that naturally populate your intestinal tract — may help prevent weight gain and actually fight obesity, which now plagues more than one-third of all Americans.

Dr. Jeffrey Gordon and his colleagues made this important discovery after observing the effects of intestinal germs implanted into several groups of pathogen-free mice. WU graduate student Vanessa Ridaura, who worked alongside Dr. Gordon for the study, took gut bacteria from four pairs of twins, each of which included both an obese and a lean sibling. One pair of the twins was also identical, which was meant to rule out any possibility that weight differences might somehow be inherited.

The team transplanted gut bacteria from these eight individuals into the intestines of young mice, which were specifically bred to lack their own natural bacteria, and watched for variations in how these mice developed over time. In the end, it was noted that the mice who received gut bacteria from the obese individuals tended to not only gain more weight than the other mice but also undergo some serious metabolic changes that left them significantly more unhealthy.

What helped further prove that the bacterial source made all the difference was the fact that all the mice ate the same amount of food, and yet only those implanted with the obese bacteria experienced weight gain and health deterioration. The reason, say experts, is that obese people tend to harbor a less diverse array of beneficial bacteria in their guts, while leaner people possess the bacterial variations and balance necessary to maintain a proper and healthy weight.

But the findings do not stop here. After performing this first set of experiments, the team decided to put mice from both the lean and obese groups into cages with one another to observe how cross-exposure to different bacterial profiles might affect the mice’s health and weight. For those who are unaware, mice tend to eat feces, which contain intestinal bugs and other markers of gut composition.

Not surprisingly, this grouping of the mice and the resultant exposure to varying bacterial profiles led to a phenomenon called bacterial swapping, in which bacteria from each of the mice comingled with one another to create new bacterial profiles. But what came as a surprise was the fact that bacteria from the lean mice invaded the intestines of the obese mice, triggering positive changes in both weight and metabolism.

“It was almost as if there were potential job vacancies,” explained Dr. Gordon about the apparently deficient bacterial profiles of the obese mice. At the same time, the positive changes observed in the obese mice were not reciprocal in the lean mice, meaning the introduction of bacteria from the obese mice did not result in any negative changes in the lean mice.

According to Michael Fischbach from the University of California, San Francisco, who was not involved in the study but spoke to The New York Times about it, these findings provide “the clearest evidence to date that gut bacteria can help cause obesity.” Adding to this sentiment, Dr. Jeffrey S. Flier from Harvard Medical School told reporters that the findings, which were recently published in the journal Science, are “pretty striking.”

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Healthy gut bacteria prevent obesity: Study

Can Bacteria Fight Obesity? Gut Bacteria From Thin Humans Can …

fat-mouse-bannerfat-mouse-banner

Why are some people fat? It’s not just a question that fat people ask themselves, but also one that drives much medical research because obesity increases the risk of serious illnesses including heart disease and diabetes.

A study recently published in Science adds gut bacteria to the list of possible causes of obesity.

The intestine is home to trillions of microbes that help the body break down and use food. The particulars of the mix have been found to vary significantly from person to person, even among identical twins.

Gordon-RidauraGordon-RidauraIn an effort to isolate the contribution of gut bacteria to weight, researchers led by Jeffrey Gordon, of Washington University in St. Louis took the bacteria from pairs of identical and fraternal twins, each with one obese twin and one lean, and put it in previously germ-free cloned mice. (We glossed tastefully over the matter of the fecal transplant.)

The results indicate that bacteria does in fact play a powerful role: The mouse that got the obese twin’s bacteria grew fat and developed metabolic problems linked to insulin resistance, even when fed only low-fat mouse chow.

The researchers then housed the fat and thin mice together, allowing their gut bacteria to mix. (Mice housed in the same cage typically eat each other’s droppings.) The thin bacteria beat out the fat bacteria in the obese mice, and they became thin again.

So is obesity purely a question of gut bacteria? No such luck. The “thin” bacteria, specifically a group called Bacteroidetes, was only able to triumph when the fat mice were eating low-fat mouse chow. When they were fed a higher-fat food meant to mimic a typical American diet, obese mice kept the obese twin’s gut bacteria — and the excess weight.

Bacteroides biacutisBacteroides biacutis

Bacteroides biacutis

“Eating a healthy diet encourages microbes associated with leanness to quickly become incorporated into the gut. But a diet high in saturated fat and low in fruits and vegetables thwarts the invasion of microbes associated with leanness. This is important as we look to develop next-generation probiotics as a treatment for obesity,” said Gordon.

It can’t be long before we see Bacteroidetes and other potentially thinning “probiotics” for sale in the supermarket next to green tea.

But, buyer beware, the mouse studies are far from conclusive. The next step for Gordon and his team will be growing microbes in the lab and mixing them to nail down which combinations have which metabolic effects.

“There’s intense interest in identifying microbes that could be used to treat diseases,” he said.

Especially diseases that make us fat.

Photos: Lexicon Genetics Incorporated via Wikimedia Commons; Gordon with graduate student and co-author Vanessa Ridaura, E. Holland Durando, Washington University of St. Louis; CDC via Wikimedia Commons

Low diversity of gut bacteria linked to heart disease, obesity


By Staff Writer
NYR Natural News

Natural Health News — New research shows that there is a link between number and diversity of bacterial species in the gut and the risk of chronic disease.

An international consortium of researchers report that overweight people with fewer bacterial species in their intestines are more likely to develop complications, such as cardiovascular diseases and diabetes. In addition, a gut with decreased bacterial richness appears to function entirely differently to the healthy variety with greater diversity.

Says lead researcher Jeroen Raes from the University of Brussels: “This is an amazing result with possibly enormous implications for the treatment and even prevention of the greatest public health issue of our time.”

Diversity is the key

Gut bacteria strengthens our immune system, produces vital vitamins and communicates with the nerve cells and hormone-producing cells within the intestinal system. The researchers add that gut bacteria also produces a variety of “bioactive substances” which enter the bloodstream, affecting our biology.

The gut needs a wide diversity of intestinal bacteria in order to maintain all these processes. In the current study people who were overweight were more likely to have low diversity in their gut flora.

The bacterial link

In this current study researchers took a closer look at the intestinal flora of 169 obese Danes and 123 non-obese Danes. The results were published in the journal Nature.

According to Raes “We were able to distinguish between two groups based on their intestinal flora: people with a large richness of bacterial species in their intestines and people with a fewer bacterial species. A species-rich bacterial flora appeared to function differently compared to the poorer variety. It was surprising to see that obese and non-obese people were found in both groups.”

The scientists found that the group with lower species richness in their intestinal flora was more susceptible to developing obesity-related conditions and chronic inflammation.

In addition, the obese people in this group were more at risk of cardiovascular conditions than the obese people in the other group. These are important results that suggest that it is not only weight gain and dietary habits that play a role in the development of medical complications in obese people.

Chicken and egg?

Metabolic conditions have become an epidemic partly due to the modern sedentary lifestyle and the and easy access to large amounts of energy-dense food. It is expected that obesity will increase tremendously all over the world; from 400 million obese people in 2005, to more than 700 million in 2015.

Some people appear to be more vulnerable to putting on eight than others and many studies over the years have examined the possible cause of this.

The researchers say they do not know whether lack of intestinal bacteria is the cause of obesity, or whether obesity causes a decrease in intestinal bacteria.

However, previous research has also suggested a link between gut bacteria and obesity. A study from the Cedars-Sinai Medical Center in Los Angeles, for example, found that certain types of bacteria in the gut cause it to take more calories from food, therefore leading to weight gain.

Dietary measures

Another finding of the international study was that a quarter of the participants had 40% fewer gut bacteria genes and correspondingly fewer bacteria than average.

Extrapolated to the entire population this suggests that a low number and diversity of gut bacteria could play a major role in health problems.

They say they cannot yet explain fully why some people have fewer intestinal bacteria compared with others, but they believe our diet may be a contributing factor.

They point to a 2012 study from a French research team, which revealed that a group of overweight participants who followed a low-fat diet for 6 weeks and who had fewer intestinal bacteria at the beginning of the diet, showed an increase in gut bacteria in both variety and amount.

“Our intestinal bacteria are actually to be considered an organ just like our heart and brain, and the presence of health-promoting bacteria must therefore be cared for in the best way possible. Over the next years, we will be gathering more knowledge of how best to do this.”

Obesity could be caused by bacteria: French study

Is obesity caused by something other than the common explanations of a bad diet and lack of excercise? According to a new study carried out in France the probelem could be linked to levels of bacteria in the gut.

Obesity and the medical problems it causes could be linked to a lack of good bacteria in the gut according to findings of a new study in France.

Many believe obesity is caused by nothing other than poor diet and lack of exercise but the findings of the latest French-Danish study by the National Institute of Agricultural Research (INRA), based in Paris point to a low count of a certain kind of “good” bacteria in the gut as another possible cause.

The study, carried out in both France and Denmark and published in scientific journal Nature, found a link between obesity and people with a low number of good bacteria present in their intestinal flora. Good bacteria are those which help digest food and fight against bad bacteria. People with a lower bacteria count were shown to be more susceptible to becoming obese.

“If you have less good bacteria, the risk of developing serious illnesses such as diabetes or cardiovascular problems is a lot higher” said Professor Dusko Erlich, the coordinator of the study.

Erlich added that the results were important because “we think that if we manage to replace these bacteria, it could help prevent excessive weight gain.” However, he admits that scientists first need to learn “how to cultivate the bacteria, which we are unable to do right now.”

Researchers studied 123 non–obese and 169 obese Danish people. They discovered that amongst the subjects studied, the people who had a greater presence of good bacteria in their intestines, had a greater resistance diseases like diabetes.

They also found that the obese people with less bacteria put on more weight than obese people with more intestinal bacteria.

Obesity is a major issue for Western countries, who are undertaking new studies to tackle the problem. In 2005 it was estimated that 500 million people were obese and this number looks set to rise to 700 million by 2015, reported French TV station Europe 1.

In a second study published in the same journal, researchers found that a diet rich in fibre and fruit and vegetables followed over a course of 12 weeks could significantly improve intestinal flora and increase the good bacteria in the gut, thus reducing some health complications linked to obesity.

This supports previous research showing that changes to diet can have direct effects on bacteria in the gut.

by Naomi Firsht

(news@thelocal.fr)

What do you think? Leave your comment below.

Your Gut Bacteria May Predict Your Obesity Risk – WebMD

Your Gut Bacteria May Predict Your Obesity Risk

By Randy Dotinga

HealthDay Reporter

WEDNESDAY, Aug. 28 (HealthDay News) — Bacteria in people’s digestive systems — gut germs — seem to affect whether they become overweight or obese, and new research sheds more light on why that might be.

The findings, from an international team of scientists, also suggest that a diet heavy in fiber could change the makeup of these germs, possibly making it easier for people to shed pounds.

“We know gut bacteria affect health and obesity, but we don’t know exactly how,” said Dusko Ehrlich, a co-author of the two new studies and coordinator of the International Human Microbiome Standards project.

The research finds that “people who put on the most weight lack certain bacterial species or have them at very low levels. This opens ways to develop bacterial therapies to fight weight gain,” he said.

Experts believe the gut, where the body processes food, is crucial to weight gain and weight loss.

“It is now well known that bacteria in our gut play an important role in our health and well-being, possibly as important as our own immune response and proper nutrition,” said Jeffrey Cirillo, a professor at Texas AM Health Science Center’s department of microbial pathogenesis and immunology. “This means that disruption of the bacteria in our gut by use of antibiotics or eating foods that help only particular bacteria grow can have effects upon our entire bodies.”

A study released last March in the journal Science Translational Medicine suggested that gastric bypass surgery led to weight loss — in mice — because it changed the makeup of the bacteria in their intestines.

In one of the new studies, which are both published in the Aug. 29 issue of the journal Nature, researchers analyzed the gut bacteria of 169 obese Danish people and 123 Danish people who were not obese.

The gut germs in the obese people were less diverse than in the others, and had more abnormalities in terms of metabolism. Also, obese people with a less diverse supply of germs gained more weight.

It’s not clear how the bacteria and obesity are related. But the research suggests that the metabolisms of the germs themselves are connected to the overall metabolism in the humans where they live, Cirillo said.

The finding could also have a practical application, the researchers said.

“The study lays ground for a simple test, which should tell people what their risk for developing obesity-linked diseases is,” study co-author Ehrlich said. If they are, he said, diet changes may be necessary.

In a second study, researchers monitored gut bacteria as 49 overweight and obese people tried to lose weight with diets that were low-fat and low-calorie but high in protein plus fiber-rich foods like vegetables and fruits. The diet appeared to actually change the bacterial makeup in the guts of the participants.

“Although these are relatively early and small studies on the topic, they suggest that management of our own diets can improve the richness of the flora within our guts and decrease our chances of becoming obese,” said Cirillo. “This does not mean that changes in diet will be effective for all people or that they can prevent obesity no matter how much someone eats, but that they can help the situation.”

Good gut bacteria could protect obese people from heart disease and diabetes …

  • Scientists have discovered a link between obesity-related diseases and levels of bacteria found in the intestines
  • They also found that gut flora with low levels of bacterial diversity functions differently to those with a variety of microorganisms
  • Results
    suggest it is not only weight gain and dietary habits that play a role
    in the development of medical conditions in obese people

By
Emma Innes

13:18 EST, 28 August 2013


|

13:18 EST, 28 August 2013

Good bacteria in the gut protect obese people from heart attacks and strokes, according to scientists.

A study has found a link between the medical problems caused by being overweight, and the bacterial species in the intestines.

People with less of these bugs are more likely to develop metabolic disorders such as cardiovascular diseases and diabetes.

Good bacteria in the gut protect obese people from heart attacks and strokes, according to scientists

Good bacteria in the gut protect obese people from heart attacks and strokes, according to scientists. People with more good bacteria are less likely to develop heart disease and diabetes

A flora with decreased bacterial richness seems to function entirely differently to the healthy variety with greater diversity.

Professor Jeroen Raes, of Vrije University in Belgium, said: ‘This is an amazing result with possibly enormous implications for the treatment and even prevention of the greatest public health issue of our time.

‘But we are not there yet. Now we need studies in which we can monitor people for a longer period.’

Metabolic conditions are becoming endemic because of people failing to exercise and eating foods that are high in sugar and fat.

It is expected obesity levels will nearly double from 400 million in 2005, to more than 700 million in 2015 – and the trend is expected to persist at least until 2030.

Professor Raes and his colleagues examined the intestinal flora of 169 obese and 123 non-obese Danes and found those with low species diversity had more metabolic abnormalities, such as increased body fat and insulin resistance.

A flora with decreased bacterial richness seems to function entirely differently to the healthy variety with greater diversity

A flora with decreased bacterial richness seems to function entirely differently to the healthy variety with greater diversity

Professor Raes said: ‘We were able to distinguish between two groups based on their intestinal flora: people with a large richness of bacterial species in their intestines, and people with less bacterial species.

‘A species-rich bacterial flora appeared to function differently compared to the poorer variety. It was surprising to see obese and non-obese people were found in both groups.’

The scientists found the group with lower species richness in the intestinal flora were more susceptible to developing obesity-related conditions and chronic inflammation.

The obese people in this group were more at risk of cardiovascular conditions than the obese people in the other group.

The results are important because they suggest it is not only weight gain and dietary habits that play a role in the development of medical complications in obese people.

In a second study published in the same journal, Professor Stanislav Ehrlich of the National Institute of Agronomic Research in Jouy-en-Josas, France, showed eating plenty of fruit and vegetables can boost gut microbes.

He looked at 49 obese or overweight individuals and found increasing consumption of high-fibre foods led to more bacterial richness and improved some clinical symptoms associated with obesity.

The finding supports previous research linking diet composition to the structure of gut microbe populations – and suggests a permanent change may be achieved through adopting an appropriate diet.

A QUARTER OF PEOPLE LACK HEALTHY LEVELS OF GUT BACTERIA

Humans have about 3.5lbs of bacteria living in their intestines, according to a new study.

However, a quarter of people have guts which house fewer bacteria than they should do to ensure we stay healthy.

One in four people are lacking the healthy bacteria which help break down our food and maintain a healthy digestive system, scientists have discovered.

Experts looking at intestinal bacteria from 292 people in Denmark found that about a quarter of people have up to 40 per cent less gut bacteria than average.

These people are more likely to be obese and suffer from mild inflammation in the digestive tract and in the entire body.

This is known to affect metabolism and increase the risk of type 2 diabetes and cardiovascular diseases.

Author of the study Oluf Pedersen, professor and scientific director at the Faculty of Health and Medical Sciences, University of Copenhagen, says we need plenty of bacteria in our guts in order to improve our health.

He compares the human gut and its bacteria with a tropical rainforest and explains that we need as much diversity as possible, and – as is the case with the natural tropical rainforests – decreasing diversity is a cause for concern.

In the study, which is published in the scientific journal Nature, Professor Pederson said: ‘It appears that the richer and more diverse the composition of our intestinal bacteria, the stronger our health.

‘The bacteria produce vital vitamins, mature and strengthen our immune system, and communicate with the many nerve cells and hormone-producing cells in the intestinal system.

‘And, not least, the bacteria produce a wealth of bioactive substances which penetrate into the bloodstream and affect our biology in countless ways.’

The comments below have not been moderated.

I’ve just finished a course of antibiotics and am having some natural yoghurt with breakfast each day to try to restore my good bacteria – still don’t feel so good – so I’m wondering whether to lash out the $30 or so for some refrigerated probiotics – I had once before and felt great soon after – hmm – maybe …

Frankly
,

Sydney, Australia,
29/8/2013 02:22

Kefir is one of the options. Lactofermentation is another one. people have been doing it for centuries. It is easy, it is cheap, you can do it. The only thing, you have to get over your fear of bacteria instilled in you by the advertising of antibacterial products.

Margareth
,

LV,
28/8/2013 22:54

In response to ‘Thomas. Hexham, UK’ there’s much research (finally!) into the importance of the human microbiome (our unique mix of gut/ intestinal bacteria) in relation to our health. The best ways – in my opinion – to increase the ‘good’ bacteria is to eat a balanced diet,* very* much limiting processed foods and sugars especially. Also, avoid broad spectrum antibiotics (which wipe out good bacteria and allow bad bacteria to flourish) unless absolutely necessary. Finally, find a really good broad probiotic – a good one will help to repopulate your gut with a diverse range of the ‘good’ bacteria.

Rachel_NZ
,

Auckland,
28/8/2013 22:48

Does a lack of the ‘right’ bacteria cause obesity, or does obesity cause a lack of the ‘right’ bacteria?

Norfolk Dumpling
,

Great Yarmouth,
28/8/2013 22:37

I’d be more interested in the different enzymes present and variations in their expression over time and on specific diets. There is great difficulty isolating all the bacteria present in the gut flora whereas the enzymes they produce can be easily measured. Also, it would be necessary to know which enzymes- even different types of the same enzyme so methods of identifying these would be required.

It seems odd if they haven’t used this approach which is called metabolomics/proteomics because it is agreed for many areas of microbial ecology to be the best. It will lead to more very interesting information about the role of gut flora particularly any links to cancers in the gut and diet and other gastoenteric diseases as well as modulation of the immune response.

ken mist
,

paris,
28/8/2013 22:37

I got my water Kefir off ebay for 3 quid, been using it for over a year now and never looked back, cleared up my acne too

Mark
,

Sheffield,
28/8/2013 22:27

The generational legacy of taking antibiotics for everything, including things they don’t help/cure.

MyOpinionIsDifferent
,

GrowUp, United Kingdom,
28/8/2013 22:18

Non of it will replace a good diet and exercise. It’s not rocket science and it takes effort.

worried for the future
,

Leeds England,
28/8/2013 22:08

As someone else said – kefir. Google it. I make my own.

Brighton Boy
,

Brighton sometimes,
28/8/2013 22:07

Good bacteria is really relating to taking a good probiotic supplement daily and eating lots of live yogurt .

petra
,

Sandon,
28/8/2013 22:05

The views expressed in the contents above are those of our users and do not necessarily reflect the views of MailOnline.

Obesity-Cancer Link Explained By 'Gut Bug' Changes, New …

Print Friendlyobese moujse, lean mouse

Changes in the gut microbiome could help explain why obese mice are more likely to develop liver tumors (inset).
Credit: Eiji Hara/Japanese Foundation for Cancer Research

A long-standing question in medical science has been explaining the obesity-cancer link in humans; previous studies have shown that obesity increases the risk for many illnesses such as diabetes and cancer. But the exact biological mechanism that underlies this link has been elusive.

But now, a new study of mice microbiomes (the communities of trillions of microbes that live in the digestive tract) has revealed a DNA-damaging acid that seems to be the key molecule linking excess weight to cancer.

Researchers at the Cancer Institute at the Japanese Foundation for Cancer Research in Tokyo discovered that obesity in mice alters their microbiota — their intestinal “bug” population — which in turn leads to the unregulated production of an acid molecule called deoxycholic that can cause damage to a cells DNA and eventually cancer (e.g., liver cancer).

To uncover the elusive link, the team — led by Eiji Hara — studied two groups of mice: one lean group that was fed a normal diet, and a second group fed a fat-heavy diet (making them obese). To induce cancer in the mice (which normally don’t get much cancer) they exposed both groups to a cancer causing chemical shortly after birth.

Results of these experiments revealed the identical obesity-cancer link noted in humans: only 5% of the mice in the lean group developed cancer later in life, whereas all the obese mice did. But this result does not mean that diet itself is the primary trigger; when the team reproduced the experiment with mice that were genetically altered to become obese (though fed a normal diet), they found that these mice had an increased incidence of cancer. This seems a clear indication that it is obesity, rather than diet, that made the difference.

Pinning Down the Causal Mechanisms

The researchers found that the obese mice were more prone to live cancer and analysis of their tumors showed increased levels of key signaling molecules called pro-inflammatory cytokines which, as the name suggests, promote inflammation (note: Inflammation has been strongly correlated with tumorogenesis in many studies, but whether it is the cause, or effect, of cancer is still debated).

The team also observed that the obese mice had higher levels of deoxycholic acid (DCA), which is a cellular by-product that results when gut microbes break down bile acid (which is manufactured in the liver). The DCA has been shown previously to damage DNA and is associated with some human cancers.

With the confirmation of these two indicators (the elevated DCA and cytokine levels), the researchers next analyzed the mice intestinal tracts. Intriguingly, they observed that the obese mice were host to a different mixture of gut bugs. Specifically, they found that a type of bacteria known as gram-positive bacteria (which have a single, thick cell wall) were far more prevalent in the fatter mice.

When the team treated the obese mice with an antibiotic (vancomycin) that targets gram-positive bacteria, the result was reduced levels of DCA and a reduced incidence of cancer. Further, when they directly targeted the DCA — by slowing bile acid breakdown or stimulating more bile acid secretion into the gut — they again found a reduced incidence of cancer (and giving them increased doses of DCA brought the cancer risk back up).

“I was very surprised by the process,” Hara says. “We never expected that changes in the gut microbiota could cause the higher risk of cancer.” [source]

The gut microbiota has been the focus of intense research just in the past two years and researchers have noted many links between the composition and activity of our microbiomes and various diseases (such as inflammatory bowel disease, certain allergies, and heart disease).

These recent findings by Hara et al lend additional support to the once controversial ‘germ theory” of cancer causation: that bacteria can be primary contributors to the development of cancer (note: the helicobacter pylori bacterium was  shown to cause stomach cancer nearly a decade ago). These results may help doctors better predict — and even prevent — the disease.

However, more research is needed to demonstrate that the same mechanisms are at work in humans, who possess different cellular “micro-environments” than mice.

Results of the experiments were reported on-line June 26, 2013, in the journal in Nature.

Some source material for this post cam from the Science NOW article:‘Gut Bugs Could Explain Obesity-Cancer Link’ by Gisela Telis

 

 

Michael Ricciardi (362 Posts)

Michael Ricciardi is a well-published writer of science/nature/technology articles and essays, poetry and short fiction. Michael has interviewed dozen of scientists from many scientific fields, including Brain Greene, Paul Steinhardt, and Nobel Laureate Ilya Progogine (deceased).
Michael was trained as a naturalist and taught ecology and natural science on Cape Cod, Mass. from 1986-1991. His first arts grant was for production of the environmental (video) documentary ‘The Jones River – A Natural History’, 1987-88 (Kingston, Mass.).
Michael is also an award winning, internationally screened video artist. Two of his more recent short videos; ‘A Time of Water Bountiful’ and ‘My Name is HAM’ (an “imagined memoir” about the first chimp in space), and several other short videos, can be viewed on his website (http://www.chaosmosis.net).
Michael currently lives in Seattle, Washington.

Breath Test Might Predict Obesity Risk – WebMD

Breath Test Might Predict Obesity Risk

By Denise Mann

HealthDay Reporter

TUESDAY, March 26 (HealthDay News) — A simple breath test may be able to tell if you are overweight or will be in the future, a new study suggests.

According to the findings, results from a standard breath test used to assess bacterial overgrowth in the gut can also tell doctors if you have a high percentage of body fat.

The microbiome, or the trillions of good and bad bugs that line your gut, can get out of balance. When bad bacteria overwhelm good bacteria, symptoms such as bloating, constipation and diarrhea may occur. The new study, appearing in the April issue of the Journal of Clinical Endocrinology Metabolism, suggests that this scenario may also set someone up for obesity.

For the study, individuals drank a sugary lactulose syrup. Breath samples were then collected every 15 minutes for two hours. Participants also had their body fat measured in two ways. One was body mass index (BMI), which takes height and weight into account. The other method uses low-wattage electrical conductivity, which differentiates between lean and fatty tissue.

Those participants whose breath samples showed higher levels of two gases — methane and hydrogen — had higher BMIs and more body fat than participants who had normal breath or a higher concentration of only one of the two gases, the study showed. This pattern suggests that the gut is loaded with a bug called Methanobrevibacter smithii, the researchers explained.

It’s possible that when this type of bacteria takes over, people may be more likely to gain weight and accumulate fat, said lead study author Dr. Ruchi Mathur, director of the outpatient diabetes treatment center at Cedars-Sinai Medical Center in Los Angeles.

Although there are other ways to measure body fat and BMI, the researchers suggested that individuals with higher methane and hydrogen content in their breath may be more likely to respond to specific weight loss methods down the line. “Obesity is not a one-size-fits-all disease,” Mathur said.

If the study findings are confirmed, certain weight-loss treatments could be matched to people who have this breath pattern. One possibility, for instance, might be that probiotics, which help restore and maintain the natural balance of organisms in the gut, could have a role in treating or preventing obesity.

But the science is not there yet, experts cautioned.

“This is an important study looking at bacteria in the intestine and how they are related to BMI,” said Dr. Spyros Mezitis, an endocrinologist at Lenox Hill Hospital in New York City. “The more methane and hydrogen in the breath, the higher the body fat.” But, “we need more studies to figure out how bacteria is related to the growing obesity epidemic and what happens if we modify it,” Mezitis said.