LNT vs Hormesis and adaptive response = both are industry arguments. Hormesis is a religion. Adaptive response – lets damage a cell, oh looks it tries to fix itself. Lets damage it some more- oh look it tries even harder to fix itself. ALL ARE INDUSTRY ARGUMENTS – LNT – less slack regulation. Hormesis – no regulation. adaptive response a medical concept which is unworkable outside lab but which is used by industry to justify leaving contamination unremediated and for u mining and enrichment and for leaving children in contaminated areas around the world. Including Fukushima.

Brief extracts:



N.E. Gentner and R.V. Osborne

Atomic Energy of Canada Limited, Canada


There is a vigorous debate about whether or not there may be a “threshold” for radiation-

induced adverse health effects. A linear-no threshold (LNT) model allows radiation

protection practitioners to manage putative risk consistently, because different types of

exposure, exposures at different times, and exposures to different organs may be summed.

If we are to argue to regulators and the public that low doses are less dangerous than we

presently assume, it is incumbent on us to prove this. The question is, therefore, whether

any consonant body of evidence exists that the risk of low doses has been over-estimated.

From the perspectives of both health physics and radiobiology, we conclude that the

evidence for linearity at high doses (and arguably of fairly small total doses if delivered at

high dose rate) is strong. For low doses (or in fact, even for fairly high doses) delivered at

low dose rate, the evidence is much less compelling. Since statistical limitations at low

doses are almost always going to prevent a definitive answer, one way or the other, from

human data, we need a way out of this epistemological dilemma of “LNT or not LNT, that

is the question”. To our minds, the path forward is to exploit (1) radiobiological studies

which address directly the question of what the dose and dose rate effectiveness factor is

in actual human bodies exposed to low-level radiation, in concert with (2) epidemiological

studies of human populations exposed to fairly high doses (to obtain statistical power) but

where exposure was protracted over some years.

The issue we have to address and

rectify is in large part to narrow the band within which estimates of any risk at low doses and low dose

rates must lie. Untenable generalizations will not help.

Evidence that no

significant effect is seen (one way or the other) ought not to be misconstrued as evidence that there is no effect. Thus, despite claims to the contrary, most low dose studies are not “proof of no effect” but rather “no proof of effect”.

The 1994 UNSCEAR

conclusions—that extensive data “provide no evidence to support the view that the adaptive response in cells decreases the incidence of late effects in humans after low doses”, and that “at this stage it would be premature to draw conclusions for radiological protection purposes” (UNSCEAR 1994b)—remain valid.

the question of import for threshold

versus non-threshold is whether a single track of ionizing radiation can induce the necessary damage in a target tissue. (Note that it is not necessary that every such single track be able to do this, only that the there be a non-zero probability). Evidence exists for all types of ionizing radiations that a single track can induce a wide array of lesions in DNA, including the double-strand breaks implicated as critical damage (see, e.g., Goodhead, 1994).

However, a radiation event may affect how the cell or its associated tissue handles non-radiation-related but potentially deleterious events that occur sufficiently soon and close enough. One could therefore have an increase in some deleterious effects, and a reduction in others because of a general increase in repair capability. What the net effect might be depends on many biological variables so that simple generalizations one way or the other are unlikely to be valid.


there also exist persons with various syndromes associated with diminished repair capability, including for ionizing radiation-induced damage. Hence risk in some persons, and possibly in some tissues in most persons, may well extend down to very low doses.


A considerable array of genes has been identified that is associated with increased risk of cancer. Only a

portion of these seem to relate to DNA repair. These cancer genes (present in a fraction of the population) may account for a considerable fraction of human cancer.

We conclude therefore that even if the overall risk might decrease to zero in some persons at low doses and/or low dose-rates, it is unlikely to be the case for all persons, and it may well not be the case for the subset of persons who may normally give rise to most cancers in a population. That is, there likely will always be some individuals at enhanced risk, however low the dose.

The “Problems” the LNT Hypothesis Cause are Addressable

The “problems with LNT theory” mainly relate to what are seen as excessive costs for protection against

radiation versus other risks to human health. The issue as we see it is that the attention given to low doses of radiation is excessively high even if the LNT-based risk coefficients were to be correct. This is the issue we have to continue to address and rectify. It is this cost of a theoretical cancer death prevented that is out-of-whack; public misperception and whatever leads to this misperception—not LNT—is to blame for this. To be effective, it is the perception issue that has to be addressed.

However, while the lung

cancer risk was negated by this fractionated exposure, it must be emphasized that no such protection was seen for breast cancer: this cohort exhibited a risk comparable with that seen in the ABS, and there was no evidence of protection by dose fractionation (Howe and McLaughlin, 1996).

What if there was a threshold dose?
First, we would have to make the practical assumption that we do not have a detailed accounting of any individual’s complete personal dose history, nor of their genetic make up, nor of their individual cellular responsiveness to radiation at any particular time.

Then, given the multitude of factors influencing radiation response, the only practical and equitable

approach is to associate with increments of radiation dose from man-made sources (or any other) a

probability of advancing an individual (whose position in the distribution we do not know) towards a

deleterious biological response. The only reasonable assumption for a hypothetical individual somewhere in the distribution is that the bigger the dose, the proportionately bigger the likelihood of an advance towards an effect. (Note, this does not preclude that in some individuals from any particular additional radiation dose, there may be no actual effect, a much greater actual deleterious effect, or a beneficial actual effect, or even both some deleterious and some beneficial effects.). Such an approach protects the hypothetical average individual, accepting that we do not know the characteristics of each individual, only the estimated bounds of response from epidemiology.


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