Innovations in modern medicine have helped improved life expectancy and quality of life, however, sometimes, drugs or treatments eventually fail. Researchers used mathematical models to explain the evolutionary process of treatment resistant depression.
Treatment resistance occurs when a drug doesn't work on patients anymore. This is commonly caused by repeated medications, wrong dosages or misdiagnosis, however, it is also linked to genetic mutation. Previously, bet-hedging has been acknowledged as a drug resistance mechanism in bacterial infections and cancers.
"Treatment resistance occurs partly because cell populations are heterogeneous -- consisting of a mixture of cells with differing characteristics, some of which are impervious to therapy," said Dr. Alexander Anderson of Oxford University according to Science Daily.
It was unclear how the bet-hedging phenomenon first evolved. Bet-hedging occurs when an organism suffers in normal conditions, in turn, its adaptability is improved in extremely stressful conditions. In a study published in the December 2016 issue of Genetics closely explains the biological systems of bet-hedging using mathematical modeling, which is not possible using clinical experiments.
The researchers found out that bet hedging is caused by biological redundancy which leads to genetic mutations. It initially does not have an impact on the characteristics of a species but the mechanism which controls bet-hedging can slow the rate of its loss. These results are especially important in treating treatment resistant depression.
The study suggested a way to overcome in treating treatment resistant depression though so-called treatment holiday. This involves stopping the treatment for some time before resuming it. "One strategy with the potential to overcome resistance is called a treatment holiday, wherein a patient ceases treatment for a period of time," Dr. Dan Nichol from Oxford University and the study's lead author said. He added that this is to prevent strong selection for drug resistant cells that might cause a relapse.