X-rays, Cancer and Heart Disease

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April 07, 2001 | 36,118 views

John Gofman, M.D., Ph.D., is one of the leading experts in the world in these issues. He is a nuclear physicist and a medical doctor.

The evidence presented in his book, Radiation from Medical Procedures in the Pathogenesis of Cancer and Ischemic Heart Disease, strongly indicates that over 50% of the death-rate from Cancer today, and over 60% of the death-rate from Ischemic Heart Disease today, are x-ray-induced.

The finding means that x-rays (including fluoroscopy and CT scans) have become a necessary co-actor -- - but not the only necessary CO-actor -- - in causing most of the death-rate from Cancer and from Ischemic Heart Disease (also called Coronary Heart Disease, and Coronary Artery Disease).

In multi-cause diseases such as Cancer and Ischemic Heart Disease, more than one necessary CO-actor per fatal case is very likely. Absence of any necessary CO-actor, by definition, prevents such cases. The concept of x-ray-induced cases means cases which would be absent in the absence of exposure to x-rays.

X-rays and other classes of ionizing radiation have been, for decades, a proven cause of virtually all types of mutations -- - especially structural chromosomal mutations (such as deletions, translocations, and rings), for which the doubling dose by x-rays is extremely low. Additionally, x-rays are an established cause of genomic instability, often a characteristic of the most aggressive Cancers.

Not surprisingly, a host of epidemiologic studies have firmly established that x-rays and other classes of ionizing radiation are a cause of most varieties of human Cancer. We have a high level of confidence that our findings, about the important causal role of medical radiation in both Cancer and IHD, are correct.

Reduction of exposure to medical radiation can and will reduce mortality rates -- - from Cancer with certainty, and with very great probability from Ischemic Heart Disease too.

Part 2. Some Key Facts about X-rays and Ionizing Radiation in General

Most physicians and other people appreciate the imaging capability of the x-ray, but -- - through no fault of their own -- - they are taught very little about the biological action of those x-rays which never reach the film or other image-receptor.

Capacity To Commit Mayhem Among The Genetic Molecules

The biological damage from a medical x-ray procedure does not come directly from the x-ray photons. The damage comes from electrons, which those photons "kick" out of their normal atomic orbits within human tissues. Endowed with biologically unnatural energy by the photons, such electrons leave their atomic orbits and travel with high speed and high energy through their "home cells and neighboring cells.

Each such electron gradually slows down, as it unloads portions of its biologically unnatural energy, at irregular intervals, onto various biological molecules along its primary track (path).

The molecular victims include, of course, chromosomal DNA, and the structural proteins of chromosomes, and water. Even though each energy-deposit transfers only a portion of the total energy of a high-speed high-energy electron, the single deposits very often have energies far exceeding any energy-transfer which occurs in a natural biochemical reaction. Such energy-deposits are more like grenades and small bombs

The Free-Radical Fallacy

There is no doubt that, along the path of each high-speed high-energy electron described above, the energy-deposits produce various species of free radicals. Nonetheless, it is a demonstrated fallacy to assume equivalence between the biological potency of x-rays and the biological potency of the free radicals which are routinely produced by a cell's own natural metabolism.

The uniquely violent and concentrated energy-transfers, resulting from x-rays, are simply absent in a cell's natural biochemistry. As a result of these "grenades" and "small bombs," both strands of opposing DNA can experience a level of mayhem far exceeding the damage, which metabolic free-radicals (and most other chemical species) generally inflict upon a comparable segment of the DNA double helix.

Ionizing Radiation: A Uniquely Potent Mutagen

The extra level of mayhem is what makes x-rays (and other types of ionizing radiation) uniquely potent mutagens. Cells cannot correctly repair every type of complex genetic damage, induced by ionizing radiation, and sometimes cells cannot repair such damage at all. Not all mutated cells die, of course. If they all died, there would be very little Cancer and no inherited afflictions. Indeed, certain mutations confer a proliferative advantage on the mutated cells. Exposure to x-rays is a proven cause of genomic instability -- - a characteristic of many of the most aggressive Cancers.

Unlike some other mutagens, x-rays have access to the genetic molecules of every internal organ, if the organ is within the x-ray beam. Within such organs, even a single high-speed high-energy electron, set into motion by an x-ray photon, has a chance (far from a certainty) of inducing the types of damage which defy repair. That is why there is no risk-free (no safe) dose-level .

There is widespread agreement that, by its very nature, ionizing radiation at any dose-level can induce particularly complex injuries to the genetic molecules. There is growing mainstream acknowledgment that cellular repair processes are fallible, or entirely absent, for various complex injuries to the genetic molecules.

The Very Low Doubling-Dose for X-ray-Induced Chromosomal Mutations

The inability of human cells, to repair correctly every type of radiation-induced chromosomal damage, has been demonstrated in nuclear workers (who received their extra low-dose radiation at minimal dose-rates) and in numerous studies of x-ray-irradiated human cells at low doses.

Besides demonstrating non-repair or imperfect repair, such studies have established that x-rays have an extremely low doubling-dose for structural chromosomal mutations. (The doubling dose of an effect is the dose, which adds a frequency equal to the preexisting frequency of that effect.)

For instance, the doubling-dose for the dicentric mutation is in the dose range delivered by some common x-ray procedures, such as CT scans and fluoroscopy -- - i.e., in the dose range of 2 to 20 rads. The rad is a dose-unit which is identical to the centi-gray. We, and many others, prefer the simpler name: Rad.

X-rays are capable of causing virtually every known kind of mutation -- - from the very common types to the very complex types, from deletions of single nucleotides, to chromosomal deletions of every size and position, and chromosomal rearrangements of every type. When such mutations are not cell-lethal, they endure and accumulate with each additional exposure to x-rays or other ionizing radiation.

Medical X-rays as a Proven Cause of Human Cancer

Ionizing radiation is firmly established by epidemiologic evidence as a proven cause of almost every major type of human Cancer. Some of the strongest evidence comes from the study of medical patients exposed to x-rays -- - even at minimal dose-levels per exposure.

Mounting mainstream evidence indicates that medical x-rays are 2 to 4 times more mutagenic than high-energy beta and gamma rays, per rad of exposure.

No Doubt about Benefits from Medical Radiation

Radiation was introduced into medicine almost immediately after discovery of the x-ray (by Wilhelm Roentgen) in 1895.

There is simply no doubt that the use of radiation in medicine has many benefits. The findings in this book provide no argument against medical radiation. The findings do provide a powerful argument for acquiring all the benefits of medical radiation with the use of much lower doses of radiation, in both diagnostic and interventional radiology.

(Interventional radiology refers primarily, but not exclusively, to the use of fluoroscopy to acquire information during surgery and during placement of catheters, needles, and other devices.)

Within the professions of radiology and radiologic physics, there are mainstream experts who have shown how the dosage of x-rays in current practice could be cut by 50%, or by considerably more, in diagnostic and interventional radiology -- - without any loss of information and without eliminating a single procedure.

Role of Medical Radiation in Causing Cancer and IHD, Past and Present

This monograph has produced evidence with regard to two hypotheses.


Medical radiation is a highly important cause (probably the principal cause) of cancer mortality in the United States during the Twentieth Century. Medical radiation means, primarily but not exclusively, exposure by x-rays -- - including fluoroscopy and CT scans. (Hypothesis-1 is about causation of Cancer, so it is silent about radiation-therapy used after a Cancer has been diagnosed.)


Medical radiation, received even at very low and moderate doses, is an important cause of death from Ischemic Heart Disease (IHD); the probable mechanism is radiation-induced mutations in the coronary arteries, resulting in dysfunctional clones (mini-tumors) of smooth muscle cells. (The kinds of damage to the heart and its vessels, observed from very high-dose radiation and reported for decades, seldom resemble the lesions of IHD)

These Hypotheses in Terms of Multi-Cause Diseases

Cancer and Ischemic Heart Disease are well established as multi-cause diseases. In efforts to prevent these multi-cause diseases, reduction or removal of any necessary CO-actor is a central goal. The evidence in this book is that medical radiation has become a necessary CO-actor in a high fraction of the U.S. mortality rates from both diseases. Fortunately, dosage from medical radiation is demonstrably reducible without eliminating a single procedure.

The Database for Dose: Physicians per 100,000 Population

During the 1985-1990 period, the number of diagnostic medical x-ray examinations performed per year in the USA was approximately 200 million, excluding 100 million dental x-ray examinations and 6.8 million diagnostic nuclear medicine examinations.

The source of these estimates warns that 200 million could be an underestimate by up to sixty percent.

Not only is the number of annual examinations quite uncertain, but the average doses per examination -- - in actual practice, not measured with a dummy during ideal practice -- - vary sometimes by many-fold from one facility to another, even for patients of the same size. The variation by facility has been established by a few on-site surveys of selected facilities, because measurement and recording of x-ray doses are not required for actual procedures.

Fluoroscopy is a major source of x-ray dosage, because the x-ray beam stays "on" during fluoroscopy. Such doses are rarely measured.

When fluoroscopic x-rays are used during common diagnostic examinations, the total dose delivered varies with the operator. When fluoroscopic x-rays are used during surgery and other nondiagnostic procedures, the total dose delivered varies both with the operator and the particular circumstances.

Our monograph is essentially the first, large prospective study on induction of fatal Ischemic Heart Disease by medical radiation. The results are stunning in their strength. Such strong dose-response relationships do not occur by accident.

Our Unified Model of Atherogenesis and Acute IHD Events

Our view (shared by many others) is that the plasma lipoproteins have no physiologic function in the intimal layer of the coronary arteries, and that under normal circumstances, their rate of entry and exit from the intimal layer is in balance. We propose that what disrupts this lifelong egress of lipoproteins from the intima -- - with the disruption occurring only at specific locations -- - are mutations acquired from medical radiation and from other mutagens.

In our Unified Model, some mutations acquired by smooth muscle cells render such cells dysfunctional and give such cells a proliferative advantage -- - so that they gradually replace competent smooth muscle cells at a localized patch of artery (a mini-tumor). And this patch of cells, unable to process lipoproteins correctly, becomes the site of chronic inflammation, resulting in construction of an atherosclerotic plaque -- - whose fibrous cap is sometimes too fragile to contain the highly thrombogenic lipid-core within the plaque.

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