Dysbiosis & Dysregulated Metabolism: Are the bugs in our belly making us fat?
Wendee Holtcamp’s article (1) in this month’s Environmental Health Perspectives (EHP) covers the provocative argument that dysbiosis (altered gut microbes) contributes to disordered metabolism, causing us to gain weight and develop metabolic disorders like diabetes. Holtcamp notes, “The microbiota that populate human intestinal tracts vary substantially from person to person, and mounting evidence suggests these interindividual variations in gut microbiota affect how a person metabolizes chemicals they may be exposed to.”
Her summary is based on a timely review (2) in EHP by Suzanne M. Snedeker (Department of Microbiology and the Institute for Comparative and Environmental Toxicology) and Anthony G. Hay (Department of Food Science) from Cornell University in Ithaca, New York. The authors detail the evidence linking environmental alteration of gut ecology and human energy metabolism. It has become evident that toxins including air pollutants, plasticizers, and heavy metals, along with certain pharmaceuticals, are disrupting the balance of gut microbes, leading to inflammation and impairing our ability to regulate fat storage, gather energy from food sources and affect satiety (how full we feel) by negatively impacting hormone levels that control our appetite.
Snedeker and Hay’s results are as follows:
Mounting evidence indicates that gut microbiota composition affects obesity and diabetes, as does exposure to environmental chemicals. The toxicology and pharmacology literature also suggests that interindividual variations in gut microbiota may affect chemical metabolism via direct activation of chemicals, depletion of metabolites needed for biotransformation, alteration of host biotransformation enzyme activities, changes in enterohepatic circulation, altered bioavailability of environmental chemicals and/or antioxidants from food, and alterations in gut motility and barrier function.
These findings, as the authors point out, have tremendous consequences and point the way toward strategies to combat the rising rates of obesity, diabetes and metabolic syndrome. Two clear approaches emerge. One, we must continue to limit exposure to obesogens – toxins, chemicals and pharmaceuticals (i.e. mercury, BPA, antibiotics) that disrupt gut microbes and energy metabolism – in adults and in children. Pregnant women are of particular concern, given mounting evidence (3) linking in utero toxin exposures with epigenetic alterations, leading to fetal programming that contributes to adult onset metabolic disease and obesity. In simpler terms, what our mothers (and fathers, for that matter) are exposed to while we are fetuses not only impacts our health as infants and children but as adults. Two, pre- and probiotics clearly modify gut microbiota and have been demonstrated to alter gut inflammation and metabolism (4). It may be that delivering specific pre- and probiotics at certain colony counts may protect gut integrity and lesson the impact of environmental toxins on energy metabolism. I think taking a high quality, high colony count (minimum 5-10 billion CFU) probiotic daily would be a good start. Again, the timing of this intervention may be crucial, as studies (5) of prenatal probiotics on childhood weight gain have yielded complex findings that bear replication and demand further investigation.
Citations
1. Holtcamp W: Gut Check: Do Interactions between Environmental Chemicals and Intestinal Microbiota Affect Obesity and Diabetes? Environ Health Perspect. 2012 Mar;120(3):a123.
2. Snedeker SM, Hay AG: Do interactions between gut ecology and environmental chemicals contribute to obesity and diabetes? Environ Health Perspect. 2012 Mar;120(3):332-9.
3. Slomko H, Heo HJ, Einstein FH: Minireview: epigenetics of obesity and diabetes in humans. Endocrinology. 2012 Mar;153(3):1025-30.
4. Hakansson A, Molin G: Gut microbiota and inflammation. Nutrients. 2011 Jun;3(6):637-82.
5. Luoto R, Kalliomäki M, Laitinen K, Isolauri E: The impact of perinatal probiotic intervention on the development of overweight and obesity: follow-up study from birth to 10 years. Int J Obes (Lond). 2010 Oct;34(10):1531-7.
