[ RadSafe ] POLITICALLY, "Assume No Repair"?! - in 'How Low Doses Of Radiation Can Cause Heart Disease And Stroke'

Fri Oct 23 14:05:43 CDT 2009

Faith, Monty et al. God provides. People heal (and we medics claim credit). 

These authors ASSUME NO, "Reaction to Injury" (the title of my Pathology text by Forbus) 

The following excerpt from its Discussion, does not even appear in the Abstract, also below. This is is as politically motivated as the Global Warming hoax 

(oops, it is "Climate Change", now that modeled alarmism is refuted by - the weather!) 

At age 82, I sit on thoriated welding rods to bring my vitamin R level up to Denver's, where there is much less cancer and heart disease than here in SF Bay Area. 

At Doctors for Disaster Preparedness meetings, my classmate Pollycove, B. Cohen, Luckey, Cameron, Luan and others have shown with epidemiology, animal experiments, bomb survivor, NSMS, Taiwan apt (natural experiment) etc. the 

clear benefit from ~10 rem/yr apparently from stimulation of that repair, as with allergy shots. 

Howard Long MD MPH 

A Model of Cardiovascular Disease Giving a Plausible Mechanism for the Effect of Fractionated Low-Dose Ionizing Radiation Exposure 

[FROM DISCUSSION 

-However, as we note below, because of cellular repair processes, which are not taken into account in our model , [emphasis by Long] 

 there are reasons for assuming that perturbation by radiation would not be instantaneous, so that this process might be extended over at least a period of hours after exposure.]  

INTRODUCTION 

Atherosclerosis is the main cause of coronary heart disease and stroke, the two major causes of death in developed society. There is emerging evidence of excess risk of cardiovascular disease in various occupationally exposed groups, exposed to fractionated radiation doses with small doses/fraction. The mechanisms for such effects of fractionated low-dose radiation exposures on cardiovascular disease are unclear. We outline a spatial reaction-diffusion model for early stage atherosclerotic lesion formation and perform a stability analysis, based on experimentally derived parameters. We show that following multiple small radiation doses the chemo-attractant (MCP-1) concentration increases proportionally to cumulative dose; this is driven by radiation-induced monocyte death. This will result in risk of atherosclerosis increasing approximately linearly with cumulative dose. This proposed mechanism would be testable. If true, it also has substantive implications for radiological protection, which at present does not take cardiovascular disease into account. The major uncertainty in assessing low-dose risk of cardiovascular disease is the shape of the dose response relationship, which is unclear in high dose data. [HERE IS THE POLITICS - THE FINALE OF THE INTRODUCTION AND THE ABSTRACT!] 

  Our analysis suggests that linear extrapolation would be appropriate. 

            Mark P. Little * , Anna Gola , Ioanna Tzoulaki 

Department of Epidemiology and Public Health, Faculty of Medicine, Imperial College London , London , United Kingdom 

Abstract  Top 

Atherosclerosis is the main cause of coronary heart disease and stroke, the two major causes of death in developed society. There is emerging evidence of excess risk of cardiovascular disease at low radiation doses in various occupationally exposed groups receiving small daily radiation doses. Assuming that they are causal, the mechanisms for effects of chronic fractionated radiation exposures on cardiovascular disease are unclear. We outline a spatial reaction-diffusion model for atherosclerosis and perform stability analysis, based wherever possible on human data. We show that a predicted consequence of multiple small radiation doses is to cause mean chemo-attractant (MCP-1) concentration to increase linearly with cumulative dose. The main driver for the increase in MCP-1 is monocyte death, and consequent reduction in MCP-1 degradation. The radiation-induced risks predicted by the model are quantitatively consistent with those observed in a number of occupationally-exposed groups. The changes in equilibrium MCP-1 concentrations with low density lipoprotein cholesterol concentration are also consistent with experimental and epidemiologic data. This proposed mechanism would be experimentally testable. If true, it also has substantive implications for radiological protection, which at present does not take cardiovascular disease into account. The Japanese A-bomb survivor data implies that cardiovascular disease and cancer mortality contribute similarly to radiogenic risk. The major uncertainty in assessing the low-dose risk of cardiovascular disease is the shape of the dose response relationship, which is unclear in the Japanese data. The analysis of the present paper suggests that linear extrapolation would be appropriate for this endpoint. 

----- Original Message ----- 
From: "Monty Charles" <m.w.charles at bham.ac.uk> 
To: "Mark Ramsay" <mark.ramsay at ionactive.co.uk>, srp-uk at yahoogroups.com, "Radsafe" <radsafe at radlab.nl>, HASNET-RAD at JISCMAIL.AC.UK 
Sent: Friday, October 23, 2009 8:57:14 AM GMT -08:00 US/Canada Pacific 
Subject: [ RadSafe ] 'How Low Doses Of Radiation Can Cause Heart Disease And Stroke' 

I don't think one can be complacent about this. Evidence is slowly mounting 
in support a low dose effect (below 0.5Gy) for non-cancer diseases. One 
factor which led ICRP (Publication 103) and UNSCEAR (2006) not to 
include non-cancer risks in their general low dose risk estimates was the 
lack of an underlying biological mechanism. The paper of Little et al is worth 
a read. Their mathematical model has a reasonable biological basis and 
predicts LNT for cardiovascular disease. The authors point out the 
limitations of the the model - but it has the great virtue of being testable by 
in-vitro, animal or human studies. It gains plausibility by predicting excess 
relative risk values in line with observed values from a range of 
epidemiology studies. The mathematics will be intractable to many but the 
table which compares model  predictions with radiation epidemiology data is 
clear. 

Monty Charles 
******************************* 
> Hi Mark 
> 
> Thank you for sending the link to the article. It was not a new 
> finding. RERF has noted it among the A-bomb 
> survivors. It appears that the effect is so small that it is 
> unlikely to influence the magnitude of the currently 
> accepted risk estimates 
> 
> Regards 
> K S Parthasarathy 
> 
> ________________________________ 
> From: Mark Ramsay <mark.ramsay at ionactive. co.uk> 
> To: srp-uk at yahoogroups.com; Radsafe <radsafe at radlab.nl>; 
> HASNET-RAD at JISCMAIL.AC.UK 
> Sent: Fri, 23 October, 2009 19:19:17 
> Subject: [ RadSafe ] 'How Low Doses Of Radiation Can Cause Heart 
> Disease And Stroke' 
> 
> Hello all. 
> 
> 'How Low Doses Of Radiation Can Cause Heart Disease And Stroke' 
> 
> Not 'new news' - but latest paper published today - (cat and 
> pigeons 
> comes to mind if this is accepted). 
> 
> News article found here: http://tiny.cc/CP9Ha 
> 
> Full publication of paper found here http://tiny.cc/ssgST 
> 
> Regards 
> 
> Mark 
> 
> Mark Ramsay 
> Radiation Protection Adviser 
> 
> Email: mark.ramsay at ionactive. co.uk 
> Web: www.ionactive.co.uk 
> 
> Ionactive on Twitter 
> www.twitter.com/ionactive 
> 
> Ionactive Blog 
> www.ionactive.co.uk/blog 
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Dr Monty Charles 
Reader in Radiation Physics 
School of Physics & Astronomy 
University of Birmingham 
Edgbaston 
Birmingham B15 2TT, UK 
Tel +44(0)121 414 3483 
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