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Probiotics linked to obesity


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#1 neogenic

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Posted 23 April 2008 - 01:43 PM


I have read a few articles now in this light and I am wondering what the board's thoughts are on this topic. Clearly, this board and most life extensionist's position is pro-probiotics making your reaction to this of great interest to me.

http://www.scienceda...80401165014.htm
From Science Daily

In the April issue of Mayo Clinic Proceedings, researchers from Mayo Clinic Arizona and Arizona State University examine the role that bacteria in the human gastrointestinal tract play in regulating weight and the development of obesity.

Known as gut microbiota, the trillions of bacteria that populate the human gastrointestinal tract perform a variety of chores. These "friendly" microbes help extract calories from what we eat, help store these calories for later use, and provide energy and nutrients for the production of new bacteria to continue this work.

According to John DiBaise, M.D., a Mayo Clinic Arizona gastroenterologist and lead author of the Mayo Clinic Proceedings article, several animal studies suggest that gut microbiota are involved in regulating weight and that modifying these bacteria could one day be a treatment option for obesity.

One study cited by the authors observed that young, conventionally-reared mice have a significantly higher body fat content than a laboratory-bred, germ-free strain of mice that lack these bacteria, even though they consumed less food than their germ-free counterparts. When the same research group transplanted gut microbiota from normal mice into germ-free mice, the germ-free mice experienced a 60 percent increase in body fat within two weeks, without any increase in food consumption or obvious differences in energy expenditure.

Another animal study reviewed by the authors focused on the gene content of the gut microbiota in mice. Finding more end products of fermentation and fewer calories in the feces of obese mice led researchers to speculate that the gut microbiota in the obese mice help extract additional calories from ingested food.

"These results suggest that differences exist in the gut microbiota of obese versus lean mice, raising the possibility that the manipulation of gut microbiota could be a useful strategy for regulating energy balance in obese people," says Dr. DiBaise.

Although information on the link between gut microbiota and obesity in human subjects is more limited, the authors present some evidence supporting this connection. One study cited placed 12 obese participants in a weight-loss program for a year, randomly assigning them to either a fat-restricted or carbohydrate-restricted, low-calorie diet. Researchers noted distinct differences between lean and obese participants when they monitored the type and number of bacteria found in participants' stool samples before and after the diet changes.

Another study cited followed children from birth to age 7 and analyzed stool samples collected at 6 and 12 months. The children who were normal weight at age 7 had distinctly different bacteria in their samples from those collected from overweight-obese children, suggesting that differences in the composition of the gut microbiota precede overweight-obesity.

Dr. DiBaise says that much more research is needed to clarify a number of issues related to the relationship between the gut microbiota and obesity. Future studies need to establish whether the small changes in caloric extraction seen in recent studies can produce measurable weight differences in humans. Second, researchers need to prove or disprove the possible relationship between the gut microbiota and the regulation of weight.

"In particular, it is essential to demonstrate unequivocally whether differences in gut microbiota in obese versus lean people are the cause or the result of obesity," says Dr. DiBaise.

Finally, the authors note that the next wave of research should explore the safety and feasibility of modifying the gut microbiota in clinical trials involving humans.

"Although clearly no substitute for proper diet and exercise, manipulation of the gut microbiota may represent a novel approach for treating obesity that has few adverse effects," says Dr. DiBaise.

Other authors of this article include: Husen Zhang, Ph.D., Rosa Krajmalnik-Brown, Ph.D., and Bruce Rittmann, Ph.D., from Arizona State University; and Mayo Clinic Arizona researchers Michael Crowell, Ph.D. and G. Anton Decker, M.B.B.Ch.

#2 neogenic

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Posted 26 April 2008 - 01:45 PM

I have read a few articles now in this light and I am wondering what the board's thoughts are on this topic. Clearly, this board and most life extensionist's position is pro-probiotics making your reaction to this of great interest to me.

http://www.scienceda...80401165014.htm
From Science Daily

In the April issue of Mayo Clinic Proceedings, researchers from Mayo Clinic Arizona and Arizona State University examine the role that bacteria in the human gastrointestinal tract play in regulating weight and the development of obesity.

Known as gut microbiota, the trillions of bacteria that populate the human gastrointestinal tract perform a variety of chores. These "friendly" microbes help extract calories from what we eat, help store these calories for later use, and provide energy and nutrients for the production of new bacteria to continue this work.

According to John DiBaise, M.D., a Mayo Clinic Arizona gastroenterologist and lead author of the Mayo Clinic Proceedings article, several animal studies suggest that gut microbiota are involved in regulating weight and that modifying these bacteria could one day be a treatment option for obesity.

One study cited by the authors observed that young, conventionally-reared mice have a significantly higher body fat content than a laboratory-bred, germ-free strain of mice that lack these bacteria, even though they consumed less food than their germ-free counterparts. When the same research group transplanted gut microbiota from normal mice into germ-free mice, the germ-free mice experienced a 60 percent increase in body fat within two weeks, without any increase in food consumption or obvious differences in energy expenditure.

Another animal study reviewed by the authors focused on the gene content of the gut microbiota in mice. Finding more end products of fermentation and fewer calories in the feces of obese mice led researchers to speculate that the gut microbiota in the obese mice help extract additional calories from ingested food.

"These results suggest that differences exist in the gut microbiota of obese versus lean mice, raising the possibility that the manipulation of gut microbiota could be a useful strategy for regulating energy balance in obese people," says Dr. DiBaise.

Although information on the link between gut microbiota and obesity in human subjects is more limited, the authors present some evidence supporting this connection. One study cited placed 12 obese participants in a weight-loss program for a year, randomly assigning them to either a fat-restricted or carbohydrate-restricted, low-calorie diet. Researchers noted distinct differences between lean and obese participants when they monitored the type and number of bacteria found in participants' stool samples before and after the diet changes.

Another study cited followed children from birth to age 7 and analyzed stool samples collected at 6 and 12 months. The children who were normal weight at age 7 had distinctly different bacteria in their samples from those collected from overweight-obese children, suggesting that differences in the composition of the gut microbiota precede overweight-obesity.

Dr. DiBaise says that much more research is needed to clarify a number of issues related to the relationship between the gut microbiota and obesity. Future studies need to establish whether the small changes in caloric extraction seen in recent studies can produce measurable weight differences in humans. Second, researchers need to prove or disprove the possible relationship between the gut microbiota and the regulation of weight.

"In particular, it is essential to demonstrate unequivocally whether differences in gut microbiota in obese versus lean people are the cause or the result of obesity," says Dr. DiBaise.

Finally, the authors note that the next wave of research should explore the safety and feasibility of modifying the gut microbiota in clinical trials involving humans.

"Although clearly no substitute for proper diet and exercise, manipulation of the gut microbiota may represent a novel approach for treating obesity that has few adverse effects," says Dr. DiBaise.

Other authors of this article include: Husen Zhang, Ph.D., Rosa Krajmalnik-Brown, Ph.D., and Bruce Rittmann, Ph.D., from Arizona State University; and Mayo Clinic Arizona researchers Michael Crowell, Ph.D. and G. Anton Decker, M.B.B.Ch.


I am kind of shocked, no one has an opinion on this one and this is one of several articles I've read lately linking the two. The relationship can clearly be debated, but I thought that it'd be...well, debated.

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#3 tintinet

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Posted 26 April 2008 - 02:45 PM

Not sure I know what to make of this report, as some studies show apparent major health and longevity benefits of prebiotics and probiotics. I just started using some probiotic supplements. I'll let you know if I suddenly blimp out!

#4 Mind

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Posted 26 April 2008 - 03:20 PM

Interesting and plausible. Even if different gut microbes only extract a small percent (less than 1%) more calories, it would add up over time. Maybe it could help a few people, however, my intuition is that most obese people will remain obese even if they did change the make-up of their gut-microbiota. The primary problem is too many calories and too little exercise.

#5 bran319

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Posted 26 April 2008 - 04:22 PM

Efficient fermentation of starches could be one reason why some are more carbohydrate intolerant and prone to weight gain than others. I wonder what correlation, if any, exists with weight, diabetes and bowel disorders such as IBS and IBD.

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#6 krillin

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Posted 26 April 2008 - 08:54 PM

The fermentation products are good for us, so I'm not going to sign up for gut sterilization.

Adv Exp Med Biol. 1999;472:149-58.
Short-chain fatty acid in the human colon. Relation to inflammatory bowel diseases and colon cancer.
D'Argenio G, Mazzacca G.
Gastrointestinal Unit, School of Medicine, Federico II University, Naples, Italy.

Short chain fatty acids (SCFAs) are the end products of anaerobic bacteria break down of carbohydrates in the large bowel. This process, namely fermentation, is an important function of the large bowel; SCFAs, mainly acetate, propionate and butyrate account for approximately 80% of the colonic anion concentration and are produced in nearly constant molar ratio 60:25:15. Among their various properties, SCFAs are readily absorbed by intestinal mucosa, are relatively high in caloric content, are metabolized by colonocytes and epatocytes, stimulate sodium and water absorption in the colon and are trophic to the intestinal mucosa. While the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in ruminants, the interest in the effects of SCFAs production on the human organism has been raising in the last ten years. SCFAs are of major importance in understanding the physiological function of dietary fibers and their possible role in intestinal neoplasia. SCFAs production and absorption are closely related to the nourishment of colonic mucosa, its production from dietary carbohydrates is a mechanism whereby considerable amounts of calories can be produced in short-bowel patients with remaining colonic function and kept on an appropriate dietary regimen. SCFAs enemas or oral probiotics are a new and promising treatment for ulcerative colitis. The effects have been attributed to the oxidation of SCFAs in the colonocytes and to the ability of butyrate to induce enzymes (i.e. transglutaminase) promoting mucosal restitution. Evidence is mounting regarding the effects of butyrate on various cell functions the significance of which needs further considerations. Up until now, attention has been related especially to cancer prophylaxis and treatment. This article briefly reviews the role of SCFAs, particularly butyrate, in intestinal mucosal growth and potential clinical applications in inflammatory and neoplastic processes of the large bowel.

PMID: 10736623




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