Radiation Hormesis and Adaptive Response – Definitions.

by nuclearhistory

  • The following is taken from “Low-dose ionizing radiation exposure: Understanding the risk for cellular transformation” By L. DE SAINT-GEORGES,*

SCK•CEN, Department of Radiobiology, Mol, Belgium. Published in: Journal of Biological Regulators and Homeostatic Agents
Received:May 15, 2004\, Accepted:June 26, 2004. Full paper download link:http://www.radiationhormesis.com/RadiationHormesis/Low-dose%20ionizing%20radiation%20exposure.pdf

Quote: “Abstract: Radiation is energy transfer.When radiation has sufficient energy to removean orbital electron from its atom, an ionized atom is formed, and radiation with the capacity to do this is called ionizing radiation.The primary effect of radiation is the induction of free radicals and Reactive Oxygen Species (ROS). All the molecules in every cell of the body are potential targets,but the final effect of radiation will be mainly of concern if the molecule impaired is a molecule critical for life. ROS are also generated as a result of the aerobic respiration (metabolic ROS) in much larger
quantity than from the natural radiation background. During evolution, life has developed powerful control and repair mechanisms that greatly contribute to minimize the risks associated with the generation of free radicals and ROS. At
low irradiation doses the probability of the risk is therefore proportional to the dose, and the ALARA (As Low As Reasonable Achievable) principle seems to be a valuable goal in radioprotection policies. (JBiol Regul Homeost Agents 2004;18:96-100) ” end quote.

This abstract is included to provide the context in which the selected paragraphs I have reproduced here  serve to define Radiation Hormesis and Adaptive Response. I hope that the reader downloads the full paper to  study the complete information.

Extracted from the paper as a source of definition for Radiation Hormesis and Adaptive Response:

Quote: ” Radiation dose: Threshold or no threshold?

An important question is about a hypothetical dose threshold. Does a threshold dose, below which the risk is nil, exist? According to what has been previously said on, the essentially random interaction of radiation with various biological molecules, it appears to make sense to consider a decrease of the risk with a decrease of the dose. However, no data exist which allows us to define a threshold value.

However, at low dose not only harmful effects but also possibly beneficial effects of radiation could occur. Here it is essential but not always evident, to clearly differentiate possibly beneficial effects from the lack of noxious effects.

Adaptive response and hormesis are often mentioned to minimize the risk of radiation or sometimes to deny any adverse outcome below a dose threshold, as detailed below.

Hormesis is a hypothesis that emphasises the possible beneficial effect of low doses of radiation and claims the necessity of a low-dose exposition to get some benefits while excluding any risk. However, this concept is controversial.

According to the hormesis model, people should be exposed to low radiation dose unless it is demonstrated with certitude that there is no benefit from such exposure. The possibility of adverse effects is not even considered.

We may wonder why the proponents of the hormesis model acknowledge a radiation threshold value for harmful effects, but reject it for beneficial effects.

Considering the essentially random interaction between radiation and target molecules leading to unpredictable molecular damage, it appears surprising that at low doses only beneficial effects would occur while noxious effect would require a dose above a certain threshold. To consider hormesis as an argument against actual dose limits would only be valid if the efficacy of hormesis could be demonstrated for the effects against which one wants to protect at low radiation doses, i.e. cancer and genetic damages.

Unfortunately this is not yet demonstrated in an unequivocal way. Therefore, the hormesis model is currently not considered in radioprotection.

The theory of “adaptive response”, (not to be confused with hormesis) shows that a low dose can reduce the effect of a higher dose when administered after a short time delay. This theory is based on substantial evidence.

To reduce a risk appears beneficial, but it does not mean that the risk is eliminated. According to the “adaptive response” model, a first low dose (conditioning dose) is considered to stimulate the DNA repair mechanisms that contribute to reduce the effect of a subsequent higher dose. But the initial low dose can only stimulate the limited number of cells actually hit, the total of which in function with the dose. This situation never excludes the possibility of a transformation of one of the cells.

The next higher dose concerns all cells. Some of them having the repair mechanisms stimulated by the first conditioning dose, and may repair the damage more easily. The other cells, that were not previously hit, are not protected. The total damage can be reduced by a factor depending on the number of the cells conditioned but will always be dependent on the total number of the cells exposed to both doses.

Would the conditioning of all cells solve the question? No, because to reach such a goal we have to increase the conditioning dose and the risk remains proportional to the dose and to the number of cells irradiated.

Therefore the adaptive response does not appear to be a relevant mechanism for radiation protection because the (low) conditioning dose that defines it, also generates a risk of transformation. On the other hand the challenging dose is not a low dose.

We suggest that natural background irradiation and metabolic ROS are already stimulating toward some adaptive response by a constant stimulation of the repair mechanisms. Then it would appear that there is no need to add to this radiation burden.

Evolution, in our natural radioactive environment, is often used as an argument to support such beneficial effects of low-dose radiation. We should remember that if Evolution has led to the current scala of successfully living species, the eliminated species are unavailable to analyse the non-beneficial aspect of evolution.

Conclusion: Is a low dose radiation safe or not?

The possible different interactions between rays and target atoms, the different types of ROS and free radicals produced, the different molecules as end points of ROS and the heterogeneity of damage in the target molecules makes the effect of ionization essentially unpredictable. Therefore, it does not seem to be appropriate to predict either deleterious or beneficial effects. Any issue from primary radiation effects remains theoretically possible.

The probability of having an effect, whatever it is depends on the dose and the number of cells being hit. However, the biological consequences can vary greatly and a distinction must be made between the organism as a whole, and the fate of individual cells. Indeed the worst issue for the cell, the cell death, is probably the best issue for the organism which in this way remains protected from transformed cells.

Cellular transformation does not threaten the life of the (cell) as it results in unlimited proliferation, but it may lead to the death of the entire organism.

Even if the probability of a transformation is no more important than the probability of any other effect, we must consider that the final outcome for the organism will be more determined by cellular transformation than by any other effect on cells. For radiation protection the fate of the organism should prevail above the fate of individual cells.

The biological effects of ROS and free radicals (and hence of radiation) are ultimately determined by the effect on the biosystem that controls the enormous burden of oxidative damage that is essentially resulting from metabolic ROS.

Checking the radiosensitivity is checking the integrity and efficiency of the control biosystems, e.g. the DNA repair system, the immune system, cell cycle control, and apoptosis.

Due to space limitations, we have not considered all elements dealing with low-dose exposition. For example, Linear Energy Transfer, dose rate, bystander effect, genomic instability and questionsrelated to internal radiation emitters, were not considered. Nevertheless, this review should contribute to the understanding of the relative risk linked to low-dose and low-dose rate radiation exposure

The Linear No Threshold hypothesis should remain so far the basic guide line for the radioprotection authorities. It appears clearly that the ALARA (As Low As Reasonably Achievable) principle, which is currently the basis of radiation protection policies, should be followed as long as no relevant scientific facts provide other insights. The very weak probability of oncogenic events at low dose should reassure everybody.

If any beneficial effects from low-dose radiation should exist, we can not exclude them, there is no reason to expect a higher occurrence probability for them than for cell transformation and the one would never exclude the other possibility in other cells. Therefore, such concepts aimed to attenuate the risk perception, will only lead toward more confusion, which in turn will generate more unwarranted anxiety and will finally be totally counterproductive.” end quote.

Reprint requests to:

Dr. Louis de Saint-Georges, SCK/CEN, Radiobiology Boeretang 200 B-2400 Mol, Belgium



Secretary treasurer of European Radiation Research Society – Senior scientist


Public Company; 501-1000 employees; Research industry

19792011 (32 years)

Research Associate University of Utah Educational Institution; 10,001+ employees; Higher Education industry

July 1988August 1990 (2 years 2 months)


Belgian Nuclear Research Centre http://www.sckcen.be/

The European Radiation Research Society, contact person Dr. Louis de Saint-Georges, secretary-treasurer. The European Radiation Research Society (formerly the European Society of Radiation Biology) is an Europeannon profit organisation founded in 1959 with the aim of promoting radiation research


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