Posted on 09/06/2013 11:44:52 AM PDT by neverdem
What makes some people slender and others full-figured? Besides diet and genetics, the community of microbes that lives inside us may be partially responsible. New research on twins suggests that lean people harbor bacteria that their obese counterparts don't have. And, given the chance, those bacteria may be able to prevent weight gain. But don’t dig your skinny jeans out of the closet just yet. So far, the work has been done only in mice. What's more, the bacterial takeover requires a healthy, high-fiber diet to work, illustrating the complex relationship between diet, microbes, metabolism, and health.
Our intestines are home to at least 400 species of bacteria, and evidence is building that the balance of microbes in our internal ecosystem has far-reaching effects on health, including brain function and risk of cancer. A study last year showed that transferring gut bacteria between humans reduced insulin resistance, which is linked to obesity.
To explore how microbes differ between obese and lean people, researchers at Washington University in St. Louis took gut bacteria from four pairs of identical and fraternal twins; one sibling in each pair was lean and the other obese. Then they transplanted these microbes into mice that had no intestinal microbes of their own. The mice who got microbes from the lean twins stayed lean, the researchers report today in Science. Those that got microbes from the obese twins increased their body fat by 10% on average, even though they were eating the same amount of food.
What would happen if these two sets of microbes got mixed up in the gut, the researchers wondered. Led by microbiologist Jeffrey Gordon and graduate student Vanessa Ridaura, the team took advantage of one of the rodents' least endearing habits: They eat each other's poop. After letting this happen, the researchers discovered that microbes from the lean twins seemed to be particularly good at taking hold in the gut ecosystems of the mice that started with obesity-associated microbes. And after those bacteria moved in, the mice didn't gain weight. The most invasive species of microbes from the thin animals were in the Bacteroidetes group, which has previously been associated with leanness in mice and humans. The obese mice seemed to have unoccupied niches that the Bacteroidetes could easily move into.
To figure out what the gut bacteria might be doing, the researchers looked for bacterial genes that were active in the two kinds of mice. The heavier mice had higher levels of proteins involved in detoxification and stress responses; the lean mice expressed more genes involved in breaking down dietary fiber.
Diet, it turns out, was key to the impressive properties of the microbes from the lean twins. All the mice in the first round of experiments had been eating chow that was high in fiber and low in fat. The researchers then prepared a mouse-pellet form of an unhealthy human diet, high in fat and low in fiber, and housed svelte and heavy mice together again. They found that, with this diet, the microbes associated with leanness didn't colonize the cagemates’ intestines.
This work was rigorously done and fits in well with earlier findings, including the idea that Bacteroides may protect against weight gain, says Alan Walker, a gut microbiologist at the Wellcome Trust Sanger Institute in the United Kingdom who was not involved in the study. What's new here, he says, is that the researchers began addressing the question of how that protection might work: which species are responsible, what genes they use, and what diet they require.
"This study is an important step toward ultimately answering these questions," says microbiologist Peter Turnbaugh of Harvard University. A valuable result of this work, they both agree, is that it sets up a way to test the effects of microbial therapies on human gut bacteria (even though the bugs are living in a mouse). The authors suggest that a logical next step is to use the animals to measure the effects of particular foods or ingredients on gut ecosystems.
The mouse experiments also provide a way to test fecal transplants, which can cure a potentially fatal intestinal infection in humans and show potential for treating other conditions such as inflammatory bowel disease and obesity. There's a danger inherent in this approach: Transferring human feces into a patient's colon runs the risk of transmitting pathogens as well. Walker and the authors note that a well-tested "next-generation probiotic" consisting of known beneficial microbes delivered as a pill or other therapy could take the place of fresh feces, and this mouse system provides a way to identify the most effective bacteria, the diseases those bacteria can treat, and whether a particular diet is necessary.
"There's a major way to go before you can translate these results to humans," Walker cautions. A weight-loss probiotic isn't a simple next step, as the researchers found when they isolated 39 of the beneficial Bacteroidetes species. The mixture was unable to cause the same effects as mouse poop, possibly because the Bacteroidetes aren't acting alone and more of the microbial players need to be identified.
Somewhere there are mice living the good life at the expense of man. I’m tired of it. Either get these things to market for humans or shut these rodent Club Meds down!
Don't look at the Chinese and Japanese. Genome studies can't distinguish the two populations from each other, IIRC. This might be true for other East Asian populations, more or less.
China the highest number of diabetics in the world
There was a story years ago in the NY Times after Bloomberg got on his health nazi hobby horse. IIRC, an overweight Chinese or Japanese was 60 % more likely to get type 2 diabetes as a Causasian who was equally overweight.
Well DUH!! It's also the highest population nation in the world. And, diabetes doesn't always necessarily have anything to do with obesity.
I'm not sure that's true. Look at Asians and Africans as an example. It's rare to see an obese Asian, whether in Asia or in America. Most of them eschew the garbage diet that government meddlers and left-field "nutritionists" have cooked up for us.
What you're missing is that it's the crappy diets - the high carb, high calorie, high-artificial fat, nutrition-free foods that causes the metabolic imbalances.
People eat crap, and it messes up their metabolism, resulting the preferential partitioning of energy into fat storage, and away from muscles and other tissues. So people get fat, while at the same time the rest of their body is starving. So they are hungry, and they are lethargic, while simultaneously they are putting on weight.
It's not that they are eating too much, it's that what they've been eating has messed up their metabolism.
Now as for the Asian cultures that eat a lot of carbs, and don't suffer from these diseases - what they don't eat is sugar or industrial seed oils. Their diets are noticeably lacking in fructose. And generally, people with healthy metabolisms can thrive on quite a lot of carbs. What they can't do is get 20% of their calories from high fructose corn syrup and 20% of their calories from industrial seed oils, and 20% of their calories from refined white flour, and keep their healthy metabolisms.
You don't need Atkins-levels of carb restrictions to stay healthy. You need Atkins-levels of carb restrictions to become healthy, after decades of eating crap has made you sick.
So, what are we supposed to believe?
Just eat real food. You know, the stuff you find in the produce section or at the meat counter. Stuff that doesn't come in a box, or stamped with a bar code. Stuff you buy fresh, and eat fresh, because it spoils if you leave it sitting out.
I never would have thoughht of that, but I didn't wrie the title. /s
And, diabetes doesn't always necessarily have anything to do with obesity.
How many of those with type 2 diabetes and normal weight are really latent autoimmune diabetes in adults and insulin dependent? Whether it's slightly overweight or morbid obesity, the typical type 2 is not skinny.
Bump to the top.
Very interesting article!
I know you uised the word "typical", but I'm going to quibble a bit with you over this. IMO (and I'm no expert), the medical folks are still trying to figure out how the body works. Classifying someone as a "typical diabetic" isn't necessarily a valid observation.
Case in point, I'm a type 2 diabetic. There is no history of diabetes in my family and I have never been morbidly obese. So, how did I become a diabetic? I, along with tens of thousands of other guys, was exposed to Agent Orange in Vietnam. And, diabetes is at the lower end of the diserases associated with Agent Orange.
I make this point because we have a belief in this country that those who are diabetic probably over ate junk food or we eat a lot of sugar. While those are "typical" causes of type 2 diabetes, there are other factors that play a part. As you noted one-third of obese people will never develop diabetes.
From all of my discusions with my doctors and clinicians over the years, I know this - we still have a long way to go to really understand the human body and why things happen the way they do. Until that day arrives, it is, again IMO, a bit early to try to fit people into specific categories based on common factors. We aren't there yet.
Makes sense, as some varieties may secrete apatite increasing hormone analogs to get the host to provide more food. Compare to toxoplasma gondiii and a bunch of other bugs that modify host behavior (rabies, etc.)
Now here's an FR exclusive, assuming it doesn't get pulled again:
Wouldn't it be interesting if a variety that makes the host hungrier thrived on fructose preferentially over varieties that thrive on sucrose?
It's pretty clear that high fructose corn syrup is associate with obesity, and with increased calorie consumption.
This could be why.
And if so, it hints at an effective treatment.
You heard it here first.
“Or we could eat veggies and go for a walk “
BARF!!!!
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