to detect the effects of low level radiation than a smaller study that properly compensates for smoking prevalence. Given the absence of direct epidemiological evidence, there is considerable debate as to whether the dose-response relationship <100 mSv is supralinear, linear (LNT), has a threshold, is sub-linear, or whether the coefficient is negative with a sign change, i.e. a hormetic response. The radiation adaptive response seems to be a main origin of the potential hormetic effect. The theoretical studies indicate that the adaptive response is responsible for the shape of dose-response curve and can transform the linear relationship (LNT) into the hormetic one. While most major consensus reports and government bodies currently adhere to LNT, the 2005 French Academy of Sciences-National Academy of Medicine's report concerning the effects of low-level radiation rejected LNT as a scientific model of carcinogenic risk at low doses. Using LNT to estimate the carcinogenic effect at doses of less than 20 mSv is not justified in the light of current radiobiologic knowledge. They consider there to be several dose-effect relationships rather than only one, and that these relationships have many variables such as target tissue, radiation dose, dose rate and individual sensitivity factors. They request that further study is required on low doses (less than 100 mSv) and very low doses (less than 10 mSv) as well as the impact of tissue type and age. The Academy considers the LNT model is only useful for regulatory purposes as it simplifies the administrative task. Quoting results from literature research, they furthermore claim that approximately 40% of laboratory studies on cell cultures and animals indicate some degree of chemical or radiobiological hormesis, and state: ...its existence in the laboratory is beyond question and its mechanism of action appears well understood. They go on to outline a growing body of research that illustrates that the human body is not a passive accumulator of radiation damage but it actively repairs the damage caused via a number of different processes, including: Mechanisms that mitigate reactive oxygen species generated by ionizing radiation and oxidative stress. Apoptosis of radiation damaged cells that may undergo tumorigenesis is initiated at only few mSv. Cell death during meiosis of radiation damaged cells that were unsuccessfully repaired. The existence of a cellular signaling system that alerts neighboring cells of cellular damage. The activation of enzymatic DNA repair mechanisms around 10 mSv. Modern DNA microarray studies which show