For a long time, we have suggested that the right microbial balance in the gut may be important for weight loss. Now a new study adds strong proof that the right gut microbiota very helpful for those who want to lose weight.
In a brilliantly conceived study by Drs. Jeffrey Gordon, Vanessa K. Ridaura and colleagues, gut bacteria from human twins, discordant for obesity – one obese, the other lean – were transplanted into mice. Mice grew fat when they got the bacteria from fat twins, and the mice that got bacteria from the lean twins stayed slim.
Here is the study summary:
Gut Microbiota from Twins Discordant for Obesity Modulate Metabolism in Mice Science 6 September 2013:
Vol. 341 no. 6150
DOI: 10.1126/science.1241214 Vanessa K. Ridaura et al
Establishing whether specific structural and functional configurations of a human gut microbiota are causally related to a given physiologic or disease phenotype is challenging. Twins discordant for obesity provide an opportunity to examine interrelations between obesity and its associated metabolic disorders, diet, and the gut microbiota. Transplanting the intact uncultured or cultured human fecal microbiota from each member of a discordant twin pair into separate groups of recipient germfree mice permits the donors’ communities to be replicated, differences between their properties to be identified, the impact of these differences on body composition and metabolic phenotypes to be discerned, and the effects of diet-by-microbiota interactions to be analyzed.
In addition, cohousing coprophagic mice harboring transplanted microbiota from discordant pairs provides an opportunity to determine which bacterial taxa invade the gut communities of cage mates, how invasion correlates with host phenotypes, and how invasion and microbial niche are affected by human diets.
Separate groups of germfree mice were colonized with uncultured fecal microbiota from each member of four twin pairs discordant for obesity or with culture collections from an obese (Ob) or lean (Ln) co-twin. Animals were fed a mouse chow low in fat and rich in plant polysaccharides, or one of two diets reflecting the upper or lower tertiles of consumption of saturated fats and fruits and vegetables based on the U.S. National Health and Nutrition Examination Survey (NHANES). (this is one of the aspects of the study we really like—giving the mice a diet that is relevant to what humans actually eat! Paul) Ln or Ob mice were cohoused 5 days after colonization. Body composition changes were defined by quantitative magnetic resonance. Microbiota or microbiome structure, gene expression, and metabolism were assayed by 16S ribosomal RNA profiling, whole-community shotgun sequencing, RNA-sequencing, and mass spectrometry. Host gene expression and metabolism were also characterized.
Results and Discussion
The intact uncultured and culturable bacterial component of Ob co-twins’ fecal microbiota conveyed significantly greater increases in body mass and adiposity than those of Ln communities. Differences in body composition were correlated with differences in fermentation of short-chain fatty acids (increased in Ln), metabolism of branched-chain amino acids (increased in Ob), and microbial transformation of bile acid species (increased in Ln and correlated with down-regulation of host farnesoid X receptor signaling). Cohousing Ln and Ob mice prevented development of increased adiposity and body mass in Ob cage mates and transformed their microbiota’s metabolic profile to a leanlike state. Transformation correlated with invasion of members of Bacteroidales from Ln into Ob microbiota. Invasion and phenotypic rescue were diet-dependent and occurred with the diet representing the lower tertile of U.S. consumption of saturated fats, and upper tertile of fruits and vegetables, but not with the diet representing the upper tertile of saturated fats, and lower tertile of fruit and vegetable consumption. These results reveal that transmissible and modifiable interactions between diet and microbiota influence host biology. Now that we know it is possible to cause weight loss through transplants of lean microbiota, a logical next step could be transplants from human to human.
But for those who don’t want to wait another minute to increase lean-producing bacteria in their gut, look at the rest of the study. The researchers found that by feeding the mice less fat, that the gut microbiota could be changed from an obese-producing microbiome to a lean one. You don’t have to wait for FDA approval to eat less fat!
If your goal is healthful weight loss, consider this important discovery: