Fwd: [ RadSafe ] CT radiation INHIBITS cancer

Mon Jan 25 15:06:55 CST 2010

Dear Dr Dachs, 

The attached ,  (permission below), 

explains my sitting on thoriated welding rods to supplement my "vit R" 

 - a  cancer-preventing, Denver-dose. 

As you will read, Feinenigan, Pollycove and Neumann's new "Low-Dose Cancer Risk Modeling --" 

is much more credible than the "frightening", Brenner' NEJM ref., 

which is entirely based on assumptions from :   

BMJ  2005;331:77 (9 July), doi:10.1136/bmj.38499.599861.E0 (published 29 June 2005) 

Risk of cancer after low doses of ionising radiation: 

retrospective cohort study in 15 countries 

E Cardis , head of radiation group 1 , M Vrijheid , scientist 1 , M Blettner , professor 2 , et al 

Results The excess relative risk for cancers other than leukaemia was 0.97 per Sv, 95% confidence interval 0.14 to 1.97. Analyses of causes of death related or unrelated to smoking indicate that, although CONFOUNDING BY SMOKING MAY BE PRESENT [emphasis by Long], it is unlikely to explain all of this increased risk. The excess relative risk for leukaemia excluding chronic lymphocytic leukaemia was 1.93 per Sv (< 0 to 8.47). On the basis of these estimates, 1-2% of deaths from cancer among workers in this cohort may be attributable to radiation. 

Conclusions These estimates, from the largest study of nuclear workers ever conducted, are higher than, but statistically compatible with, the risk estimates used for current radiation protection standards. The results suggest that there is a small excess risk of cancer, even at the low doses and dose rates typically received by nuclear workers in this study. 

 SELECTIVE,  so not credible. Instead, see (attached, 25 pp): 

Low-Dose Cancer Risk Modeling Must Recognize Up-Regulation of Protection 

(accepted for publication in   DOSE RESPONSE - 13 Nov '2009) 

    Introduction 

Epidemiology so far fails to substantiate the claim of an increase in cancer incidence in humans following low-level exposure to ionizing radiation, below about 150 mGy or mSv.  [~15 CT's - Long]  

  Rather, a decrease in cancer risk has shown up repeatedly (Pollycove and Feinendegen 2001;   Tubiana et al. 2005; Nair et al. 2009; Tubiana et al.   2009). 

Nevertheless, observed data are fitted using the linear-no-threshold (LNT) hypothesis (ICRP 1977). This hypothesis expresses proportionality between dose and risk, and is the basis for radiation protection regulation and most widely used.   

Despite contradicting epidemiological and experimental findings the LNT hypothesis is also applied to predict cancer risks of low-dose irradiation ( Brenner and Hall 2007).   What was a good intention years ago to protect workers from overexposure to ionizing radiation has been turned to producing a wide spread radiation phobia now.    

The initial plausibility of the LNT-hypothesis derived from two assumptions:   1) immediate damages to the genetic material (DNA) from radiation absorption increase in proportion to the absorbed dose; 2) certain immediate DNA damage is amplified and propagates in organisms to cause the cancer incidence in an exposed population to rise in proportion to dose.   

  The second assumption is debatable for both epidemiological and experimental reasons.   Regarding epidemiology, data show statistical constraints and require very large numbers of irradiated individuals to assess the carcinogenic risks of low doses (< 150 mSv), such large numbers are not available at present.   Thus, modeling of data with the LNT hypothesis arrives at relative risks of cancer that are actually not observed (Heidenreich et al. 1997;    Pollycove and Feinendegen 2001; Tanooka 2001; Preston et al.   2004, 2007; Cardis et al. 2007;   Nair et al. 2009;   Tubiana et al. 2009).   

The LNT hypothesis assumes its scientific justification because of the immediate linear dose-effect relationships at the molecular level of the DNA; it does not consider the complex non-linear dynamics of oncogenesis in the body.   Indeed, more recent discoveries on low-dose effects in experiments with various biological systems from cells to animals increasingly show specific responses of physiological damage control systems limited to low doses at various levels of biological organization   ( Feinendegen et al. 2004; Tubiana et al. 2005, 2009;    Mullenders et al. 2009),   and also discovered a low-dose induced reduction of the incidences of neoplastic transformation in culture cells and overt malignancies in animals ( Azzam et al. 1 996; Mitchel et al. 2003, 2008; Elmore et al . 2009).    Such responses have not been observed at, and also were not expected from, high dose radiation exposures.   In fact, new findings challenge the validity of the LNT-hypothesis, and now suggest that this hypothesis cannot be maintained (Tubiana et al. 2005, 2009; Feinendegen et al. 2007a,b). 

Currently, the discussion of the low-dose risk of cancer has become polarized on how to best incorporate new findings into practical application.   A case in point is the serious disagreement between recent statements by the French Academy of Sciences (Tubiana et al. 2005) and the US National Academy of Sciences by way of its BEIR VII report (National Research Council 2006).   

The present paper attempts to focus on the new radiobiological findings on low-dose related cancer risk.   It hypothesizes that after low dose exposures clinical cancer develops as a consequence of the balance between cancer induction and cancer prevention by the cascade of the body’s physiological defenses.    

This paper emphasizes both the proportional relationship between absorbed dose and DNA damage, and the non-linearly operating body’s defense systems that block damage propagation from the molecular level to the whole organism. There are at least three types of “defending” barriers: a physical-static one, and two metabolic-dynamic defenses.   One of the latter two defenses responds soon after perturbation, while the other involves delayed up-regulations of defenses in terms of adaptive responses that appear with a delay of hours and last for various times up to more than a year after low-dose exposure.   Adaptive protections can operate against both radiogenic and non-radiogenic DNA damage and its consequences.   Applied to the observed experimental and epidemiological data, with their wide ranges of uncertainties, the modeling indicates not only the inconsistency of the LNT hypothesis but also the high probability of beneficial, i.e., hormetic effects following low-dose irradiation ( Calabrese and Baldwin 2003). 

So, be reassured, Dr Dachs (and readers pf American Family Physician), CT rad inhibits cancer. 

Howard Long MD MPH 

Low-Dose Cancer Risk Modeling Must Recognize Up-Regulation of Protection 

(accepted for publication in   DOSE RESPONSE - 13 Nov '2009) 

    Introduction 