Stool samples transplants of course should be taken only from donors with no health issues. People who are obese have an obvious health issue. A form meant to protect the drug companies does not prove anything. They probably mention “bleeding eyeballs” and other nasty sounding side effects as well. As I said in a previous post if someone is suffering from digestive issues where they have diarrhea and are constantly pooping out almost everything they eat before their body can absorb it... there is a good chance they will gain weight when their problem goes away if they do not adjust their consumption level.
Open Forum Infect Dis. 2015 Feb 4;2(1):ofv004. doi: 10.1093/ofid/ofv004. eCollection 2015 Jan.
Weight gain after fecal microbiota transplantation.
Alang N1, Kelly CR2.
Abstract
Fecal microbiota transplantation (FMT) is a promising treatment for recurrent Clostridium difficile infection. We report a case of a woman successfully treated with FMT who developed new-onset obesity after receiving stool from a healthy but overweight donor. This case may stimulate further studies on the mechanisms of the nutritional-neural-microbiota axis and reports of outcomes in patients who have used nonideal donors for FMT.
Gut. 2017 Mar;66(3):429-437. doi: 10.1136/gutjnl-2015-310283. Epub 2016 Jan 6.
Microbiota-induced obesity requires farnesoid X receptor.
Parséus A1, Sommer N1, Sommer F1, Caesar R1, Molinaro A1, Ståhlman M1, Greiner TU1, Perkins R1, Bäckhed F1,2.
Abstract
OBJECTIVE:
The gut microbiota has been implicated as an environmental factor that modulates obesity, and recent evidence suggests that microbiota-mediated changes in bile acid profiles and signalling through the bile acid nuclear receptor farnesoid X receptor (FXR) contribute to impaired host metabolism. Here we investigated if the gut microbiota modulates obesity and associated phenotypes through FXR.
DESIGN:
We fed germ-free (GF) and conventionally raised (CONV-R) wild-type and Fxr-/- mice a high-fat diet (HFD) for 10 weeks. We monitored weight gain and glucose metabolism and analysed the gut microbiota and bile acid composition, beta-cell mass, accumulation of macrophages in adipose tissue, liver steatosis, and expression of target genes in adipose tissue and liver. We also transferred the microbiota of wild-type and Fxr-deficient mice to GF wild-type mice.
RESULTS:
The gut microbiota promoted weight gain and hepatic steatosis in an FXR-dependent manner, and the bile acid profiles and composition of faecal microbiota differed between Fxr-/- and wild-type mice. The obese phenotype in colonised wild-type mice was associated with increased beta-cell mass, increased adipose inflammation, increased steatosis and expression of genes involved in lipid uptake. By transferring the caecal microbiota from HFD-fed Fxr-/- and wild-type mice into GF mice, we showed that the obesity phenotype was transferable.
CONCLUSIONS:
Our results indicate that the gut microbiota promotes diet-induced obesity and associated phenotypes through FXR, and that FXR may contribute to increased adiposity by altering the microbiota composition.