The research points clearly in the direction of a link between a disrupted gut flora and being overweight, through energy metabolism, hormone regulation and inflammation. The evidence is predominantly associative in humans, with stronger causal indications coming from animal models. Treatments such as probiotics and faecal transplants are interesting but are still insufficiently supported by clinical evidence to justify concrete recommendations.
Yes, there is a clear association between the composition of your gut flora and being overweight, although the precise cause-and-effect relationship in humans has not yet been fully established. Multiple studies show that people with obesity have a different gut flora than people of a healthy weight. For example, bacteria from the Firmicutes group and certain Clostridium species are found more frequently in people who are overweight. These bacteria are associated with greater energy extraction from food and changes in satiety hormones, which may contribute to eating more and gaining weight. Whether this is a cause or a consequence of being overweight has not yet been fully clarified.
Gut bacteria produce substances, such as short-chain fatty acids and indole, that stimulate the production of gut hormones such as GLP-1 and GIP. These hormones are important for the feeling of satiety and for weight regulation. A disrupted gut flora can disrupt this hormone production, which may contribute to being overweight. How large this effect is in practice in humans still needs to be determined more precisely.
Another mechanism works through the intestinal wall. When the gut flora is disrupted, the intestinal wall can become permeable to bacterial building blocks known as lipopolysaccharides (LPS). These then enter the bloodstream and fuel inflammation, leading to insulin resistance, a characteristic that is closely associated with being overweight and type 2 diabetes. This mechanism is considered relevant in several review studies, although its exact magnitude in humans has not yet been accurately measured.
Research has also been conducted into the so-called gut-brain axis: through nerve pathways, hormones and the immune system, the gut flora communicates with the brain and can thereby influence eating behaviour. This sounds plausible and there are indications from animal research, but in humans this evidence is still limited. Stronger causal evidence, such as from experiments in which the gut flora of people with obesity was transferred to germ-free animals (which subsequently gained more weight), comes primarily from animal models and cannot yet be translated into direct clinical conclusions for humans.
Treatments that attempt to restore gut flora, such as faecal microbiota transplants, probiotics and prebiotics, are being investigated as a possible approach to obesity. The current state of research is promising in the sense that there are mechanistic and preliminary indications, but clinical studies in humans are still too limited in size and duration to justify concrete recommendations. At this time there is insufficient evidence to say that a specific probiotic or prebiotic reliably helps with weight management. More and larger clinical trials are needed before firm statements can be made on this subject.
All claims are based on seven PMIDs (35421277, 34321848, 29667480, 26459447, 35134709, 39673174, 39040013, 38636809), including multiple reviews and overview studies. Most human evidence is associative; causal evidence comes largely from animal models.