Drugs can be incredibly effective or complete duds in different people: One that works for me may not do anything for you. Researchers at Yale have now pinpointed the genetic and metabolic processes of our gut microbes that cause these differences. 

Gut microbes perform a variety of natural functions in the human body, from digesting the carbohydrates in your lunch to producing essential vitamins. In addition, gut microbes also interact with pharmeceuticals – sometimes irreversibly changing the active component and inhibiting its intended function. 

Evaluating how these microbes modify drugs in vivo during product development is difficult, most notably because we have not identified all the microbes, and consequentially active in our intestinal tracts. Drugs treating everything from cancer to Parkinson’s disease show strong evidence of modification or inactivation from gut microbes, and until recently the "how" and "why" of this process was unclear.

Andrew Goodman’s team at Yale University tackled this problem by developing a “gain-of-function” assay. They introduced genes from one well-known bacterial species into E. coli cells and observed which cells degraded or changed a range of chemical compounds, functions that they were not able to perform before the bacterial gene was introduced. They tested a large variety of genes from our gut bacterial microbiome to see which genes encoded enzymes that affected 271 different drugs. 

This experiment and the data they produced offer exciting potential for drug development and disease treatment. For instance, drug developers could use the data to avoid using chemical compounds that are easily digested by common gut microbes. And doctors may eventually be able to cultivate a patient's microbiome and identify the exact reason why some presciption is not working as expected, and then identify drugs that might work more effectively.