Life Extension Blood Test Super Sale

Life Extension Magazine

LE Magazine November 2001

image

Page 2 of 2

What does one particle of radiation do?

image

Some radiation terms

Rad stands for "radiation absorbed dose". A rad is the amount of radiation a person receives per gram of tissue. Ionizing radiation is photon energy that knocks electrons out of their orbits and sends them flying. The energy of the flying electrons is measured in volts. A millirad is one one-thousandth of a rad, or .001. A centi-gray (cGy) is a rad. A Roentgen is .96 of a rad, or almost a rad. X rays are radiation generated by a machine as opposed to radioactive substances, and they're essentially the same energy as gamma rays which are less than alpha rays. A source of alpha rays is radon.

In the first studies, researchers aimed a single particle at the nucleus of the cell-where DNA is located. Eighty percent of the cells shot through the nucleus survived. This contradicts the belief that if radiation slams through the nucleus, the cell will die. But the bad news is that the surviving cells contained mutations. Cells have a great capacity to repair DNA, but they cannot do it perfectly. The damage left behind in these studies from a single particle of alpha radiation doubled what damage was already there. This proved, beyond a shadow of a doubt, that there is no such thing as a safe dose of radiation. If one particle of radiation leaves damage behind-damage that can lead to cancer-then no amount of radiation is "safe". That doesn't mean that every mutation leads to cancer. The vast majority do not. But every mutation has the potential to become an abnormally growing cell, and the effects are cumulative over time.

They did more studies, hitting cells with more particles. If the cells are hit with 8 particles, about 10% of them survive, but with more damage. Twenty particles of radiation shot through one cell kills it with very few exceptions. The interesting thing about this is that a high dose of radiation that kills cells outright may be less dangerous than a lower dose that merely cripples them. Lethal hits leave no imperfectly repaired (mutated) survivors. Cells that are completely destroyed can't multiply with mutations. On the other hand, killing too many cells will kill the entire organism.

The radiation from x rays is less energetic than that from radon. But it is not less dangerous. Joint research between scientists at Brookhaven National Laboratory and the National Center for Scientific Research in France demonstrates that low LET radiation, including x rays, cause a type of damage similar to the serious double-strand breaks where radiation blasts through both strands of DNA, leaving it completely broken. The radiation from x rays causes similar damage by hitting each strand individually, but close together. The result is similar to a double strand break.

Indirect damage

What happens when an alpha particle whizzes through the cell, but misses DNA? In this case, it hits cytoplasm, the body of the cell. In 1999, Hei's group at Columbia did experiments, again shooting predetermined numbers of alpha particles through each cell. They came up with a very surprising finding. Hitting cytoplasm causes mutations in DNA. That seems odd; how could radiation damage something it doesn't touch? The answer is that radiation creates secondary free radicals. These are the types of radicals health-conscious people are familiar with. They have lower energy than radiation and they don't cause the same type of damage or as much of it. However, they can actually be worse because again, this is sublethal damage the body will attempt to repair, and mutations will inevitably result.

The body has evolved an "antioxidant defense system" to help stop these kinds of free radicals. Dietary antioxidants also help protect against them. Hei's group demonstrated that glutathione was effective, and other studies show that N-acetylcysteine, SAMe, MSM and other sulfur-containing antioxidants also protect against secondary free radicals created by radiation.

A mysterious finding

In the late '90s, it was discovered that ionizing radiation causes damage a different way. Previous research showed that adding the growth liquid from irradiated cells to non-irradiated cells could kill them. It wasn't because of free radicals or radiation damage. This is strange. Researchers at Harvard and the Los Alamos National Laboratory looked into and found that the irradiated cells might be communicating somehow with non-irradiated cells.

Meanwhile, Hei's group came up with convincing proof that irradiated cells could cause mutations in their nonirradiated neighbors. And further, that the phenomenon could be blocked by a chemical that interferes with communication between cells (lindane).

The Harvard/Los Alamos researchers also found that interfering with cellular communication stopped the damage, and this year they published proof that "bystander" cells that get no radiation at all nonetheless have changes in the expression of tumor suppressor gene p53 and a related gene that controls the cell cycle known as p21. These genes play roles in cancer. This means that radiation affects crucial genes.

The future

Researcher Hei and colleague Gloria Calaf have begun studying how breast cells respond to estrogen after being hit with alpha radiation. So far they've shown that changes occur in BRCA, the "breast cancer susceptibility gene". Researchers at Loma Linda have speeded up and worsened prostate cancer with one low-dose whole body irradiation and a growth factor. These kinds of "real world" experiments will lead to a greater understanding of radiation's contribution to cancer.

We now know that radiation damages cells in at least three different ways: directly, through free radicals and through cellular communication. The idea that there is such a thing as a "safe" dose of radiation has been disproved. Where does that leave Gofman's observation that radiation is a significant cause of heart disease and cancer? Gofman acknowledges that radiation is not the only cause of heart disease and cancer, and he's quick to point out that multiple factors contribute. Poor diet, chemicals, viruses and a lack of exercise have proven connections to heart disease and cancer, which is a multi-stage process. But far from being disproved, Gofman's observations have gained even greater support by recent radiation research. Whether we like it or not, the very thing we use for diagnosing and treating heart disease and cancer is helping cause it.

Every dose of radiation we get is cumulative. It's very important that we realize and understand that medical radiation, and indeed all radiation, is not benign. It damages tissues even though we can't feel it or see it. It can come back to haunt us years after exposure, with very serious and devastating effects. The acceptance of radiation as safe by us as individuals and by us as a society has to be challenged. Radiation is a business, an industry, not a natural part of our lives-even though we grew up believing it was. The blind acceptance of our doctor's assurances that radiation is safe-is dangerous. The blind acceptance of radiation in our society is short-sighted and potentially self-destructive.

Informed consent should become routine for radiation procedures, just as it is for other medical procedures. For this to occur, the truth about radiation has to be available to everyone-the risks as well as the benefits. No longer can we pretend that a body scan here-and-there, a chest x ray now-and-then or a quick-look-at-our-colon has no lasting effect. They do. And until we accept that, high rates of cancer and heart disease will continue, and we, ourselves, may become one of the statistics.


Books

John W. Gofman. 1996. Preventing Breast Cancer: the Story of a Major, Proven, Preventable Cause of this Disease. San Francisco: CNR Book Division.

John W. Gofman. 1999. Radiation from Medical Procedures in the Pathogenesis of Cancer and Ischemic Heart Disease: Dose-Response Studies with Physicians per 100,000 Population, 1st ed. San Francisco: CNR Book Division. (Available through www.x-raysandhealth.org).

References

Azzam EI, et al. 2001. Direct evidence for the participation of gap junction-mediated intercellular communication inthe transmission of damage signals from alpha-particle irradiated to nonirradiated cells. Proc Natl Acad Sci USA 98:473-78.

Azzam EI, et al. 1998. Intercellular communication is involved in the bystander regulation of gene expression in human cells exposed to very low fluences of alpha particles [see comments]. Radiat Res 150:497-504.

Boice JD, et al. 1977. Breast cancer in women after repeated fluoroscopic examinations of the chest. J Natl Cancer Inst 59:823-32.

Boudaïffa B, et al. 2000. Resonant formation of DNA strand breaks by low-energy (3 to 20 eV) electrons. Science 287:1658-60.

Calaf GM, et al. 2000. Establishment of a radiation- and estrogen-induced breast cancer model. Carcinogenesis 21:769-76.

Dossing M, et al. Radiation-induced lesions of the aorta (letter). Br Med J 1(6066):973.

Elkeles A. 1977. Metabolic behavior of alpha-ray activity in large human arteries: relationship to atherosclerosis. J Am Geriatrics Soc 25:179-82.

Elkeles A. 1969. Alpha-ray activity in the large human arteries. Nature 221:662-64.

Elkeles A. 1961. Radioactivity in calcified atherosclerosis. Brit J Rad 34:602-5.

Gridley DS, et al. 1997. Enhancement of prostate cancer xenograft growth with whole-body radiation and vascular endothelial growth factor. Anticancer Res 17(2A):923-8.

Hei TK, et al. 1997. Mutagenic effects of a single and an exact number of particles in mammalian cells. Proc Natl Acad Sci USA 94:3765-70.

Johnson LK, et al. 1982. Differential radiation response of cultured endothelial cells and smooth myocytes. Anal Quant Cytol 4:188-98.

Johnson LK, et al. 1982. Differential radiation response of cultured endothelial cells and smooth myocytes. Anal Quant Cytol 4:188-98.

Lauk S. 1987. Endothelial alkaline phosphatase activity loss as an early stage in the development of radiation-induced heart disease in rats. Radiat Res 110:118-28.

Loftus CM, et al. 1987. Management of radiation-induced accelerated carotid atherosclerosis. Arch Neurol 44:711-14.

Lorenz E. 1950. Some biologic effects of long continued irradiation. Am J Roentgenol 63:176-85.

Mackenzie I. 1965. Breast cancer following multiple fluoroscopies. Brit J Cancer 19:1-9.

Martell EA. 1975. Tobacco radioactivity and cancer in smokers. Am Sci 63:404-12.

Martell EA. 1974. Radioactivity of tobacco trichomes and insoluble cigarette smoke particles. Nature 249:215-17.

Martell EA. 1983. Bronchial cancer induction by alpha radiation: a new hypothesis. Proc 7th Intl Congress Rad Res, paper C6-11. JJ Broerse, et al., Ed. (Martinus Nijhoff: Amsterdam, Netherlands).

Menendez JC, et al. 1998. Effects of radiation on endothelial function. Int J Radiat Oncol Biol Phys 41:905-13.

Oh CW, et al. 2001. Induction of a senescence-like phenotype in bovine aortic endothelial cells by ionizing radiation. Radiat Res 156:232-40.

Powers BE, et al. 1999. Long-term adverse effects of radiation inhibition of restenosis: radiation injury to the aorta and branch arteries in a canine model [see comments]. Int J Radiat Oncol Biol Phys 45:753-59.

Powers BE, et al. 1999. Long-term adverse effects of radiation inhibition of restenosis: radiation injury to the aorta and branch arteries in a canine model [see comments]. Int J Radiat Oncol Biol Phys 45:753-59.

Sheehan JF. 1944. Foam cell plaques in the intima of irradiated small arteries. Arch Path 379:297-08.

Sutherland BM, et al. 2000. Clustered DNA damages induced in isolated DNA and in human cells by low doses of ionizing radiation. Proc Natl Acad Sci 97:103-8.

Tamplin AR, et al. 1970. Radiation-induced breast cancer. Lancet Feb. 7, 1970:297.

Tokunaga M, et al. 1994. Incidence of female breast cancer among atomic bomb survivors, 150-1985. Radiat Res 138:209-23.

Travis LB, et al. Mortality after cerebral angiography with or without radioactive Thorotrast: an international cohort of 3,143 two-year survivors. Radiat Res 156:136-50.

Tribble DL, et al. 1999. Ionizing radiation accelerates aortic lesion formation in fat-fed mice via SOD-inhibitable processes. Arterioscler Thromb Vasc Biol 19:1387-92.

Verheij M, et al. 1994. Ionizing radiation enhances platelet adhesion to the extracellular matrix of human endothelial cells by an increase in the release of von Willebrand factor. Radiat Res 137:202-7.

Wanebo CK, et al. 1968. Breast cancer after exposure to the atomic bombings of Hiroshima and Nagasaki. NEJM 279:667-71.

Wu L-J, et al. 1999. Targeted cytoplasmic irradiation with alpha particles induces mutations in mammalian cells. Proc Natl Acad Sci USA 96:4959-64.

Zhou H, et al. 2000. Induction of a bystander mutagenic effect of alpha particles in mammalian cells. Proc Natl Acad Sci 97:2099-104.



Back to the Magazine Forum