A Theory of Tumor and Cancer that Ensures Effectiveness of Treatment

Having substantially completed my Hub “A Theory of Heart Disease That Insures Effective Prevention, Treatment and Cure For Heart Disease" I had my eyes set on a free radical theory of tumor and cancer.

A jump from heart disease to tumor and cancer is made easier by the fact that free radicals cause mutations in DNA of the chromosome that shows as tumor or cancer. In fact, heart disease is started by free radicals causing a mutation in the DNA of a cell in the endothelium of an artery resulting in benign tumor. That tumor is called atheroma which gathers materials that grow into a plaque.

What we said about the need for a theory of heart disease is the same as that we will say for a free radical theory of tumor and cancer. A theory serves as a basis of effective prevention, treatment and cure for these diseases.

But some would say, not so fast. Especially from health professionals schooled in conventional medicine.

Conventional medicine calls cancer a non-communicable disease. It is obvious that the framework being used is the germ theory of disease involving virus and bacteria, for example. Diseases caused by microbes are communicable because microbes are transferred from the infected person to a healthy person by means of contact or by the air.

It is easy to find out if a disease is caused by a microbe by means of Koch postulates (Encyclopedia Britannica 2009). This method also pinpoints which among several microbes found in a sick person is the causal microbe.

But in tumor and cancer, no such microbe is involved. So, we should stop calling them non-communicable disease in the framework of germ theory of disease.

Why do we need a theory of tumor or cancer?

Without a theory we go about making drugs that address some aspects of the diseases only. Presently the drugs are concentrated on treatment, some on cure that are not reliable, like chemotherapy and bone marrow transplantation. Almost nothing on prevention. The main reason is that conventional medicine does not know what causes tumor or cancer. Another reason is that Big Pharma does not want people to get cured because that would reduce their market.

We start our discussion with conventional medicine because presently it is dominant. It is the mode on which most health professionals had been trained and with which consumers are familiar. It is also the basis of most tumor and cancer drugs and protocols.

“The major cause of any cancer is a mutation, or change, in the DNA of a particular type. In the case of melanoma, the cell is the melanocyte. It stands to reason that anything changing the DNA of the melanocyte cell may result in abnormal melanocyte growth and eventually cancer. So let’s look at environmental factors that may negatively affect the DNA of melanocyte cells” (Kaufman, H., MD. The Melanoma Book. 2004:25-26).

“There is evidence that when melanocyte cells are exposed to ultraviolet B rays, their DNA is damaged and they lose the ability to repair it. Once this happens, the melanocyte is unable to control its own growth, which you may recall is the beginning of cancer. The reason why we think ultraviolet B rays are an especially important risk factor in the development of melanoma and other skin cancers is because of their sunburning ability” (Same source as above, page 26).

It is noticeable that Dr. Kaufman does not pinpoint ultraviolet B rays as the cause of cancer but tags it as “the beginning of cancer,” “risk factor,” and "sunburning ability."

Of several authors I have read on tumor or cancer, Dr. Kaufman confronted the cause of tumor or cancer head on, came close to it but missed it. All of them settled on “risk factor.”

Carolyn M. Kaelin, MD, M.P.H. author of “Living Through Breast Cancer” published in 2005 did not discuss the cause of cancer but proceeded to anatomy of the breast right away.

Risk factor is not a cause

That lack of theory of tumor and cancer is similar to the lack of a theory of heart disease in conventional medicine. No cause of heart disease is tagged.

“Since we have not yet defined the precise mechanism of atherosclerosis development, it is fortunate that we can identify factors that determine people’s risk for development of the disease” (DeBakey, M. MD and A. Gotto, Jr., MD. The New Living Heart. 1997:79).

“A number of theories have been proposed to explain the development of atherosclerosis, but no single one completely and satisfactorily accounts for all the observations that have been made about this disease. To be valid, any theory about the cause and development of atherosclerosis must be consistent with what is known about its relationship to age, sex, serum cholesterol, diet, and other risk factors, and its pathological characteristics” (DeBakey, M., MD and A. Gotto, MD The Living Heart. 1977:155, authors’ italics).

“We do not have to know the exact mechanism for the development of a disease to be able to reduce risk for it. For example, the exact mechanism of lung cancer is not known, but the great majority of cases of lung cancer could be prevented through smoking cessation.”

“A risk factor is defined as any trait or habit, whether genetic or environmental (which includes lifestyle factors), that can be used to predict an individual’s probability of developing a particular disease....” (DeBakey, M. MD and A. Gotto, Jr., same source as above).

We are lucky because although DeBakey and Gotto were tackling heart disease they mentioned lung cancer, saying "the exact mechanism of lung cancer is not known." For them, that is true for lung cancer and true for all cancers.

One benefit derived from the pursuance of risk factor by Dr. DeBakey and Dr. Gotto is that they made it clear that they are not pursuing the identification of the cause of heart disease. They pursued and defined risk factor. So, we are warned not to confuse risk factor with cause as some authors do. At one time, they are talking about risk factor, at another they are talking about cause, and sometimes they make them equivalent with each other. That is a gross mistake.

Because the cause of tumor and cancer is not identified, a theory of tumor and cancer cannot be formulated. What can be formulated is a hypothesis of heart disease that cannot graduate into a theory because concepts and relationships are incomplete. Risks factors may qualify as concepts but there are no relationships among them that are verifiable or reliable. That is what is happening with heart disease insofar as conventional medicine is concerned.

For example, hypertension and cholesterol are listed as risk factors of heart disease. It is expected that if these factors were lowered, mortality due to them would decrease. A long-term study involving 610 patients was conducted in Finland. A group was given drugs that control hypertension and cholesterol, another group served as control. After several years, the mortality from heart disease among those given drugs was double that among those who were not given drugs.

Cholesterol is an unreliable predictor in heart disease (Ornish, D. MD. Dr. Dean Ornish’s Program for Reversing Heart Disease. 1996).

A free radical theory of tumor and cancer

“Free radicals and reactive oxygen species injure the deoxyribonucleic acid of mitotic cell that result in tumor and cancer.”

This formulation satisfies requirements in theory-making. It contains a minimum vocabulary, that is, it is short. No term is derived from another term (Russell, B. Human Knowledge: Its Scope and Limits. 1947). It contains concepts and relationships. A theory consists of concepts and relationships among concepts (Einstein, A. Ideas and Opinions. 1954) .

Einstein's original publication (1905) consisted of one page only, without any citation. He issued a supplement (1906) giving the formula E = mc² as a way to verify his special theory of relativity. This formula was later on verified by Enrico Fermi in 1936 and Lise Mietner and company in 1938.

The concepts are "free radical," "reactive oxygen species," "deoxyribonucleic acid," "mitotic cell," "tumor" and "cancer." The relationships are "injure," "result," and "and."

Definition of concepts

Free radical

A free radical is any atom, like oxygen atom, or molecule (molecular oxygen) or fragment of a molecule that has at least one unpaired electron (Pierce, J. Heart Healthy Magnesium. 1986). This free electron, to attain stability grabs another electron from a molecule of a tissue resulting in injury of the DNA. This injury is principally a destruction of the hydrogen bonds that abound in the DNA. The electron of hydrogen is grabbed; it is the easiest to grab because it is as strong as 5% only of the other bonds like ionic and covalent bonds (Tortora, G.F and J. Becker. Life Sciences. 1978:14). A hydrogen atom whose electron had been grabbed dies, as it were; it has no way to reconstruct itself because it consists of one electron and one proton only. That is why water is a solvent, the reason being that the hydrogen bond is easy to stretch so that other molecules can come in between molecules of water. The hydrogen bond is a bridge easy to stretch or break. Such injury shows as aberration, thickening, shortening, deletion, thinning of chromosomes of a mitotic cell that are visible in ordinary microscope. Such injury makes the cell abnormal, a mutation that may result in tumor or cancer.

It was Dr Denham Harman, MD who first made the interpretation that free radicals cause disease and aging in 1962. It was a breakthrough in medicine like the germ theory of disease inaugurated by Pasteur in 1881-84 (Cranton, E., MD. Bypassing Bypass. Updated second edition. 1995). Examples of free radicals are atomic oxygen, molecular oxygen, superoxide, singlet oxygen and ozone.

We inhale molecular oxygen and use 75% of it; we exhale the rest. Molecular oxygen used in metabolism produces superoxide. Ozone is found in the atmosphere. It is produced by sparks of electrical gadgets, and ignition of cars. Energy from the sun (ultraviolet rays) reverses the spin of one unpaired electron of molecular oxygen resulting in singlet oxygen. Other people classify singlet oxygen a reactive oxygen species; I prefer it as a free radical.

Reactive oxygen species

Reactive oxygen species (ROS) is also called reactive oxygen intermediate. It is a derivative of oxygen. For example, hydrogen peroxide. The enzyme superoxide dismutase (SOD) attaches one electron to oxygen and one hydrogen atom to form a hydrogen peroxide molecule. Hydrogen peroxide is a ROS. It acts like a free radical in that it grabs an electron from a molecule of a tissue.

During metabolism of glucose to produce energy, superoxide (O^2-) is produced as by-product. Other sources of superoxide are: (1) cyclooxygenase, (2) adenine dinucleotide dehydrogenase, an enzyme in the mitochondria, (3) xanthine oxidase, (4) nitric oxide synthase, and (5) cytotochrome P450 monooxygenase (Spieker, L. E. , A. J. Flammer and T. F. Luscher “The Vascular Endothelium in Hypertension.” The Vascular Endothelium II.2006.249-283). Superoxide is a master free radical producing several siblings.

Superoxide's reaction with nitric oxide (NO) results in peroxynitrite (ONOO^-) with one free unpaired electron. Peroxynitrite catches NO three times faster than superoxide does, reducing the supply of NO that results in inadequate dilation of arteries. This may result in angina or heart attack.

Superoxide oxidizes (destroys) L-arginine, the precursor of NO resulting in reduced supply of NO.

Superoxides react with each other, catalyzed by SOD, producing hydrogen peroxide.

Superoxides reacting with each other in the presence of iron produce hydroxyl radical, the most destructive free radical.(Sharma, H., MD. Freedom From Disease. 1993). The endothelium injured by plaque leaks iron and copper.

Superoxide oxidizes low-density lipoprotein of fats into lipid peroxide, a reactive oxygen species (ROS), that grabs a molecular oxygen with its two unpaired electrons intact resulting in another ROS. This is a chain reaction, resulting in a cascade of ROS. Lipid peroxide contributes to the plaque in heart disease.

When it takes away an electron from hydrogen peroxide, superoxide produces hydroxyl radical.

Alkoxy radical is produced when superoxides react with each other in the presence of copper.

When superoxide exceeds the threshold of SOD it produces singlet oxygen (Cranton, E., MD and A. Brecher. Bypassing Bypass. 1984:200).

Ultraviolet rays energizing water in the skin results in hydroxyl radical (Brown et al. Chemistry the Central Science. 2nd ed.).

Sources or causes of free radicals and ROS outside the body are: (1) ozone, from the atmosphere, (2) ultraviolet rays that energize molecular oxygen, the one that we breathe, into singlet oxygen. Radioactive materials from tobacco, lead 210 and polonium 210, decompose into lead 206 emitting X-rays and generating free radicals (3) nitrous oxide from pollution (4) nitrosamine or meat preservative (5) nitrobenzene, and more.

Categories in free radicals and ROS

Categories are oxidant free radicals, reactive oxygen species (ROS) and signal free radicals. An example of the latter is nitric oxide produced by the endothelium nitric oxide synthase (eNOS/NO), an enzyme. eNOS/NO is a messenger that triggers the artery to dilate and allow more blood flow. Oxidant free radicals and ROS are the destructive type if they are not neutralized or balanced out.

Trapping agents are used in free radical and ROS research. For nitric oxide, dithiocarbamate has been approved for use on human beings.

Deoxyribonucleic acid (DNA)

Let’s start from the whole picture then go to the smallest part that is functional in our level of discussion. That is, from the chromosome, down to the gene, to the nucleotide, then to hydrogen atoms.

Each cell of a human being contains 46 chromosomes; 23 came from the mother and 24 came from the father. A chromosome is a rodlike body that actually consists of two strands aligned side by side with one binder in the middle more or less; one strand is called chromatid. One chromatid came from the mother, the other from the father. A component of a chromosome is the DNA, consisting of deoxyribose sugar, phosphate and four nitrogenous bases. A deoxyribose sugar, phosphate and one nitrogenous base combine to form a nucleotide. Many nucleotides join together to form one strand that makes up one half of the DNA molecule. Two strands wind around each other like a spiral stairway to form a DNA molecule which is about two inches long.

The four nucleotides are designated as A (adenine), C (cytosine), G (guanine), and T (thymine). Three nucleotides in sequence (ACG) form a genetic code, or information code, or codon (alternative names of the same entity). ACG is one codon; CAT is another codon; AAA is another codon, and so on and so forth. A combination of codons code for an amino acid. For example, TTC and TTT code for the amino acid lysine; CGT, CGA, VGG, CGC code for alanine amino acid.

What is a gene and how does it control a part of the body?

Take the word BLUE that shows in a blue-eyed persons like Frank Sinatra or Paul Newman. Suppose B is coded by codons AAA, CCC; L is coded by codons TAT, TTT, and GAT; U is coded by codons GCT and GGG; E is coded by codons TGG and TAG. B is an amino acid; L is an amino acid; U is an amino acid; E is another amino acid. These amino acids in the sequence, BLUE, control the lens and color of the lens of the eyes of Frank Sinatra. BLUE is a gene. A gene is a combination of codons in sequence. The sequence is important.

A gene is located in the DNA molecule found in one chromatid of a chromosome. Since there are two chromatids there are two fellows of a gene that correspond with each other in the same spot in the chromatids. It’s like a zipper that consists of two strands, the teeth of one strand binds with the teeth of the other strand. In one genetic pattern, the two fellows of a gene control the same function or protein, like lens of the eyes, in the body in the same way. For example, the gene BLUE. The fellow BLUE is located in one chromatid; the fellow BLUE is located in the other chromatid. Note the bold letters. In this BLUE/BLUE gene, the color of the eyes is blue. These are called identical alleles. In another genetic pattern the two fellows in a gene control color of the eyes differently. For example, BLACK/black, the color of the eyes is black. Note the capital letters and the small letters indicating the gene. BLACK codes for the black color of the eyes; black codes for the brown color of the eyes. Here BLACK is dominant and is expressed; black is recessive and is unexpressed. The fellows of this gene are simply called alleles. So, there is a BLACK allele and there is a black allele.

The statement “Mutation means a change in a chromosome” is not specific because the chromosome has smaller parts that are in sequence. Mutation can occur in the codon (TTT,CGA) and sequence of codons (CGA,TTT). A change in the sequence means a change in the protein of a tissue. Sometimes one amino acid is substituted by another amino acid. For example, in the codons of normal hemoglobin, carrier of oxygen in the blood, glutamate is present. When glutamate is substituted by valine, a sickle cell anemia results (Cummings, M. Human Heredity, Principles and Issues. 2009).

DNA contains several hydrogen bonds that are weak, easily stretched and broken.

"...The double helical configuration (of DNA) separates, and weak hydrogen bonds between nucleotides of the unspiraled strands break. New complementary nucleotides are attached at the proper sites. Hydrogen bonds are formed between complementary nucleotides and the process of replication is completed" ('Tortora, G.J. and J. Brecker. Life Science. 1978:180, parenthetical supplied).

Free radicals and ROS can make changes in sequence of codons, and trigger substitutions of amino acids, and delete amino acids that make up the DNA. Such changes, among others, show as tumor or cancer. There are several such changes, we are showing only a few for demonstration. For more detailed discussions on this subject you may read the book "Human Heredity, Principles and Issues" by Michael Cummings (2009).

Free radicals and ROS can alter nucleotides, amino acids and the sequence of amino acids (detected by the sequencing machine).

Now we are ready for details that lead to tumor and cancer. Development of cancer takes on the two-hit model. One allele of a gene is changed or mutated that is followed by changes in the other allele.

Take the gene BRCA1, the gene that controls breast cancer. There are two forms of breast cancer; one is heritable, the other is sporadic (Cummings, M. Human Heredity, Principles and Issues. 2009). BRCA1 is a gene found in the long arm of chromosome number 17. In the heritable form, a mutated allele of gene BRCA1, indicated as BRCA1a, is inherited from one of the parents. So the sibling carries a mutated BRCA1a in each of her/his cell. But this inherited one mutation is not enough to cause breast cancer. To recall, a gene has two alleles. When the other and normal allele is also mutated in one cell, breast cancer will develop. A normal BRAC1a/BRCA1b gene binds with the protein Rap80, together they detect and repair a damage in DNA. When both alleles of BRCA1 (BRCA1a and BRCA1b) are mutated, this gene cannot bind with Rap80 and fails to repair a damage in DNA that results in breast tumor then breast cancer, according to Cummings.

The mutation of the normal allele BRCA1b is caused by environmental factors, free radicals and ROS or both. Mutation may be started by the grabbing of one electron; however, most likely by the loss of several electrons that had been grabbed.

In the sporadic form of breast cancer, both alleles (BRCA1a and BRCA1b) are normal. When both alleles are mutated by free radicals or ROS or both breast cancer develops. Breast cancer afflicts both man and woman.

Mitotic cell

They make up the body except the reproductive cells. A mitotic cell has 46 chromosomes while reproductive cells (egg and “seed” of the male) each has 23 chromosome. The egg contributes 23 chromosomes; the “seed” contributes 23 chromosome during fertilization resulting in a embryo that now has 46 chromosomes. An embryo onwards to a complete human being has stem cells and mitotic cells.

A mitotic cell duplicates itself producing two daughter cells. The new cell, if duplication had been normal, is an exact copy of the erstwhile solitary cell.

The fertilization of an egg by a "seed" of man forms an embryo that transforms in eight weeks into a fetus that grows by means of differentiation and mitosis or cell division. Differentiation is an irreversible process by which one stem cell (embryonic germ cell), designated as totipotent stem cell differentiates into pluripotent stem cells, that differentiate into multipotent cells, that differentiate into unipotent cells, that differentiate in adult cell (Bellomo, M. The Stem Cell Divide. 2006). These now produce specialized cells like skin, bone, liver, kidney, heart, eye, ear, and so forth and so on. These are all composed of mitotic cells. A mitotic cell that had sustained injury or mutation makes a duplicate that is also mutated if the mutation could not be repaired or if the repair system does not work. There are about three trillion cells in the human body, meaning three trillion copying is going on where a copying error can occur. A copying error can be repaired or it can be thrown away. Cells that replace themselves can throw away a copying error by means of apoptosis or programmed cell death. A blood cell replaces itself in 140 days. During this process the nucleus shrinks; unlike in unprogrammed cell death that involves inflammation. In apoptosis, dead cells are apoptosed by healthy neighboring cells. If injury on the DNA had piled up such that the repair system is overwhelmed, the cell does not apoptose. Its growth goes uncontrolled that may result in tumor or cancer.

There are cells that do not replace themselves, that is, they are not subject to apoptosis: brain cells, nerve cells, and cardiovascular cells consisting of heart muscles, arterial cells, veins, and capillaries. That is why a scar in the heart stays, like in rheumatic heart; a tumor in the artery remains like the atheroma that develops into a plaque; an injury in nerves remain like in Parkinson’s disease or motor neuron disease.

Tumor

Mass of cells that had grown abnormally owing to a mutation or mutations in a gene.

The development of tumor or cancer follows the double hit pattern. In heritable form, a mutated allele is inherited from one parent and the other normal allele from the other parent is also mutated. In the sporadic form both normal alleles are mutated by environmental factors, free radicals or ROS or both.

Cancer

Invasive cells that have grown abnormally owing to a mutation or mutations in a gene. Cancerous cells start colonies in other parts of the body. There is one variety called cancer in situ where new cancer cells pile on top of each other with the lump growing in size. Leukemia is unique in that it is an abnormal growth of the white blood cells, so they are mobile. Abnormal white blood cells crowd out red blood cells to such an extent that practically no oxygen is carried by the blood because red blood cells carry oxygen.

Several mutations may be involved in the development of cancer, like colon cancer. It has a heritable form like the familial adenomatous polyposis (FAP). A mutated gene called adenomatosis polyposis coli (APC) is inherited and 5 to 7 more mutations in sequence in one mitotic cell occur for colon cancer to develop. In the sporadic form, 7 mutations in sequence in genes of one mitotic cell occur caused by free radicals or ROS or both.

Let’s recap. A person with FAP has thousands of polyps in the large intestine; each polyp contains an APC/apc gene, the allele APC having been mutated. APC/apc is a notation in genetics that shows the two alleles of a gene with the same function of controlling polyp/cancer, APC being dominant, that is why it is in capital letters. Let’s follow the subsequent mutations that turns a polyp into cancer. This one polyp has a kras proto-oncogene that turns into kras-oncogone when one of its alleles is mutated. kras-oncogone turns the polyp into adenoma, "an intermediate tumor with fingerlike projections" (Cummings, M. Human Heredity, Principles and Issues. 2009:293-296). Other genes are mutated in sequence. Each new adenoma contains at least a mutated APC, a normal apc, a k-ras oncogene; gene DCC with both alleles mutated; gene DC4 with both alleles mutated; gene DPCA with both alleles mutated; and gene V18-1 with both alleles mutated. The last to mutate is p53 gene, a suppressor gene, that controls the growth of polyp. Switched on, it stops growth; switched off, the adenoma grows uncontrolled. Once p53 gene had been disabled, one adenoma would divide into two adenomas; two adenomas would divide into four polyps, and so forth and so on until the cell matrix is breached and metastasis proceeds. The adenoma graduates into colon cancer.

P53 gene can stop the adenoma from developing into colon cancer in two checkpoints. One, before the chromosome duplicates; two, before the duplicated chromosomes go into mitosis, that is, cell division to give rise to two daughter cells. In the first checkpoint, changes in the chromosome had already taken place like mutations in APC, kras-oncogene, gene DCC, etc.

What constitute the mutations in p53 gene?

"Ir is interesting to note that G.C to T.A transversions occur frequently as mutations of the p53 tumor suppressor gene in human lung, breast,, and liver cancers (e.g. Hollstein et al., 1991). More importantly, in p53, H₂O₂ (hydrogen peroxide) induces a G to T transversion at both G.residues of codon 249 (AGG) and a C to A transversion at codon 250 (CCC) (Hussain et al., 1994 (Eaton, Sandra, et al. "Free Radicals and Medicine." Biomedical EPR-Part A: Free Radicals, Metals, Medicine, and Physiology. 2005" 25-74).

That is, changes occur in the p53 gene. The information code guanine.cytosine is changed to thymine.adenine. Hydrogen peroxide, a reactive oxygen species, causes these changes.

In the sporadic form of colon cancer the normal APC/apc alleles are mutated by free radicals and/or ROS followed by mutations of other genes in the same adenoma resulting in colon cancer.

(I have a Hub “How A Polyp Develops Into Colon Cancer, Ways To Prevent And Stop This Cancer.” I keep referring to my related Hubs because Hubpages does not allow duplicates or essentially repeats between Hubs. The Hub referred to elaborates the subject in more detail).

Definition of relationships

Injure

Cause injury in nucleotide consisting of substitution, or deletion, or change in nucleotide sequence, or change in the number of chromosome; change in the chromosome consisting of aberration, shortening, thickening, thinning, or deletion.

Result in

Turn into, become, graduate into.

And

Why do we keep on saying tumor and cancer? Abnormal growth of one cell results first in tumor which is benign. That is, the mass of tumor cells do not breach the matrix that confines them. Overgrowth of tumor cells breach the matrix that confine the cell. Its bottom dissolves first, damaged by protease or bromelain that is also found in pineapple or papaya. Tumor cells escape and join the blood or lymph fluid then travel to other parts of the body, a process called metastasis. These spreading abnormal cells are now called cancer. In other words, a tumor starts in one mitotic cell. Myoma, for example, is a tumor that grows in size but does not spread; it stays where it started. Tumor cells that overgrow, escape from the matrix, and colonize other parts of the body graduate into cancer. That is why a tumor is one entity; cancer is another entity. They have the same origin but differ in composition and character. Tumor and cancer start with one mitotic cell only (Cummings, M. Human Heredity, Principles and Issues. 2009). Some people use the terms 'benign tumor' and 'malignant tumor' that refers to cancer. I prefer the straightforward terms 'tumor' and 'cancer.'

Proof

We are going to prove this hypothesis of tumor and cancer by means of arguments. It can be verified by means of experiments. One way of proof by argument is to draw a statement of fact from the hypothesis. If this statement of fact is true, it follows that the hypothesis is true. A hypothesis verified true graduates into a theory. One statement of fact is as follows:

“Free radicals cause cancer.”

This statement of fact is derived from the result of an experiment or measurement done by scientists. We are not going to conduct this experiment now; we will use the result obtained by Dr. Sharma, MD, a pathologist.

“Free radicals can be caught in the act of creating cancer by using electron spin resonance (ESR) spectrometers" [Sharma, H., MD. Freedom from Disease (How to control free radicals, a major cause of aging and disease) 1993:90]. They show as red spots.

A more specific statement of fact:

"Peroxide and/or hydroxyl radicals mutate the gene SOD1."

Superoxide dismutase (SOD) is an enzyme antioxidant that neutralizes superoxide. It has two forms: manganese SOD and copper/zinc SOD. SOD1 controls Cu/Zn/SOD; mutation of SOD1 results in the failure of Cu/Zn/SOD to scavenge superoxides in the mitochondria, the energy factory. A person whose SOD1 had been mutated becomes sick of motor neuron disease (MND) also called amyotrophic lateral sclerosis (ALS). To recall, superoxide produces several siblings called reactive oxygen species; peroxide and hydroxyl radical are among them.

The nerves and skin of a person suffering from MND deteriorate but her/his mind remains normal (Swartz H.M. et al. “Free radicals and medicine.” Eaton, S.S. et al. editors. Biomedical EPR-Part A: Free Radicals, Metals, Medicine, and Physiology. 2005:25-74). S/he becomes weak, hard of speech. MND is fatal if not cured. Conventional medicine's dealing with MND is a hit-and-miss affair because it does not recognize free radicals as causes of disease.

Another statement of fact: "Ultraviolet rays of the sun hitting the skin produces skin cancer."

This is according to Dr. Howard Kaufman, MD in his book "The Melanoma Book."

Ultraviolet rays easily produces two kinds of free radicals: singlet oxygen and hydroxyl radical. Energy of ultraviolet rays excite molecular oxygen, with two unpaired electrons, in the skin and reverse the spin of one unpaired electron resulting in singlet oxygen (Prasad, M. Heavy Metal Stress in Plants.1999:103). Singlet oxygen is more destructive than molecular oxygen because the two unpaired electron spinning in opposite direction can grab two electrons at the same time. Molecular oxygen can grab one electron at a time only owing to the parallel spin of its unpaired electrons.

When ultraviolet rays hit the water in the skin, it excites water molecules and produces H₂O⁺; the superscript (+) showing that one electron is ejected to the M orbital of oxygen. Atomic oxygen has three orbitals designated as K, L, M where M is empty but now occupied by the excited electron of water. H₂O⁺ reacts with another water molecule and produces hydromium (H₃O) and hydroxyl radical (OH^.). Notice the dot superscript (.) indicating this free radical that is different from the plain hydroxyl. Hydroxyl (H^-) is an ion originating from the dissociation of water into OH⁺ and H^- that has to do with the pH or acidity of a fluid.

Singlet oxygen and hydroxyl are mainly responsible for melanoma or skin cancer. (I have a Hub "Causes and Treatment of Melanoma (Skin Cancer, Like Colored Mole").

Still another statement of fact: "Most people who smoke contract lung cancer."

Cigarette smoke contains radioactive materials, polonium 210 and lead 210 that the tobacco plant got from the phosphate fertilizer used in raising it (Cranton, E. MD. Bypassing Bypass. Updated 2nd edition. 1995). These materials are readily available in the soil,. Lead 210 undergoes alpha particle decay into lead 206 which is stable. Lead 210 has 84 protons with corresponding 84 electrons. Two protons bump into each other and destroy each other. This decay emits energy in the form or light, X-ray, among others. The proton number is reduced to 82 while the number of electrons remains 84. The orphaned two electrons make the decaying lead 210 a free radical. The two unpaired electrons grab electrons of other molecules, DNA among others. The X-rays excite electrons of atoms in their inner orbital resulting in the change of atoms and molecules of DNA among others. Cells whose electrons had been grabbed or ejected grow in uncontrolled way that result in tumor or cancer. (I have a Hub "How Free Radicals and X-rays From Cigarette Smoke, Not Tar, Cause Cancer and Heart Disease").

We can enumerate more statements of facts supported by results of experiments or clinical trials. That can be tackled in another Hub. Other scientists may conduct experiments.

A theory explains

A theory explains (Campbell, N. What Is Science? 1921). Let’ s try this free radical theory of cancer on a phenomenon that could not be explained by Dr. Samuel S. Epstein, MD in his book “The Politics of Cancer” published in 1978, pages 159-160. He wrote that uranium miners who did not smoke and did not inhale second hand smoke developed cancer. He was dealing with tobacco or smoke as a risk factor in cancer. He did not give an explanation. Our explanation, based on the free radical theory of tumor and cancer, is as follows.

Uranium, a radioactive material, decays into lead 210 and polonium 210, among others. These two are still radioactive that decay into lead 206 that is stable.

To recall, lead 210 undergoes an alpha particle decay. It has 84 protons with corresponding 84 electrons. Two protons bump into each other and destroy each other resulting in 82 protons and 84 electrons. During the decay energy is emitted in the form or light, and x-rays, among others. Polonium 210 undergoes the same kind of decay into lead 206 (Encyclopedia Britannica 2009).

The two orphan electrons make lead 210 a free radical that causes tumor and cancer. X-rays cause changes in chromosomes that result in tumor and cancer.

Dr. Epstein, with all his good intentions, used risk factor as framework. He did not use the free radical framework which was already available.

"Equally intriguing is the potential use of aspirin in preventing colon cancer. In nonsmokers, colon cancer is the leading cause of cancer-related death...A 1991 study reported in the New England Journal of Medicine showed that regular aspirin use could reduce colon-cancer death rates in both men and women by more than 40 percent" (Sears, B., Ph.D. The Zone.1995:116).

Sears just reported the potential use of aspirin in controlling cancer; he did not explain how. Our explanation, based on the free radical theory of tumor and cancer:

The enzyme cyclooxygenase (COX) acting on arachidonic acid produces prostaglandins and superoxide. Aspirin inhibits COX from acting on arachidonic acid as substrate (Same source as above, page 113-118). It means that aspirin prevents COX from adding to the population of superoxide. Superoxide is a free radical that also produces several siblings, reactive oxygen species that act like free radicals in causing tumor and cancer.

It remains to show how interventions along the free radical theory of tumor and cancer can prevent, treat, and cure tumor and cancer. I have already done this in some of my Hubs on tumor, cancer and heart disease.

Interventions derived from the free radical theory of tumor and cancer

Prevention. Tumor and cancer can be prevented with the administration of antioxidants. The aim is not to eliminate free radicals and ROS which is impossible. It is to counterbalance them such that the oxidative stress does not occur. Antioxidants consist of supplements like vitamin A, C, E, coenzyme Q₁₀, melatonin and built-in enzyme antioxidants like superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione synthase, and catalase. Chelation therapy, oral or infusion, is an antioxidant, it also removes minerals like iron and copper that catalyze the production of ROS, hydroxyl radical and alkoxy radical. This theory make us aware and avoid free radicals in the environment like singlet oxygen, ozone and nitrous oxide. Similarly it makes us aware that treated meat like bologna, nitrosamine, meat preservatives, and other food additives produce free radicals and ROS.

The glutathione enzyme system (glutathione peroxidase, glutathione reductase, glutathione synthase) is key to the survival of man vis-a-vis free radicals. Metabolism in the body produces a lot of superoxide, the master free radical. The enzyme antioxidant SOD converts superoxide into hydrogen peroxide, a ROS. It would appear that SOD made the situation worse. However, glutathione peroxidase donates one electron to hydrogen peroxide and turns it into safe water. Glutathione reductase donates one electron to glutathione peroxidase as a replacement of the one electron it used to diffuse hydrogen peroxide (Sharma, H., MD. Freedom for Disease. 1993). Glutathione synthase makes glutathione out of glutamate, cystine, cysteine and co-factors B2, selenium, zinc and lipoic acid which the body makes (Pressman, A. and S. Buff. Glutathione: The Ultimate Antioxidant. 1998).. These elements, except lipoic acid, are available in food. That means that we can take supplements to enhance their availability. Glutamate can be obtained from carbohydrates, cysteine and cystine are available in garlic, zinc from fruits and vegetables like amaranth (an accumulator of zinc), selenium from nuts like cashew, B2 from food. We can boost our arsenal against free radicals and ROS with food available every day at low cost. Carotene or vitamin A is the only antidote to singlet oxygen; carotene is available in carrots and other natural colored food. Carotene absorbs heat, much like chlorophyll that absorbs heat from the sun and converts carbon dioxide into carbohydrates. Heat from the sun if dissipated in the body cannot produce singlet oxygen.

An enzyme antioxidants, especially those built-in in the body are recycled: SOD, glutathione system, catalase. Some supplement antioxidants can be recycled: vitamin E is recycled by vitamin C; vitamin C is recycled by NADH produced in the metabolism of glucose.

Other kinds of antioxidants die once they had donated their electrons to free radicals and ROS that is why they must be supplied continuously. Even vitamins E and C can be depleted rapidly.

Treatment. and cure. Oral and infusion chelation therapy treat tumor and cancer. Medicinal plants also treat cancer.

Recently, scientists at the University of the Philippines Manila found out that “noni juice has cytotoxic effects both on normal lymphocytes, mouse myeloma and human colon cancer cell lines that were used” (De Guzman, T; L. R. Embuscado, B. Monte, Valdez, Ma. T. 2004. “A Preliminary Study on the In vitro Anti-Cancer Potential of the Commercial Preparation and Decoction of Morinda citrifolia.” The UP Manila Journal, vol. 9, pages 42-53). Tested were commercial capsule, tea, and fresh fruits. All three extracts at 5% concentration down to 2.5% were effective on normal lymphocytes; all three at 5% down to 1.25% were effective on colon cancer; capsule extract at 5% down to 2.5% was effective on mouse myeloma cells. Lymphocyte is an antibody, a defense against foreign body invasion; myeloma is malignant tumor of bone marrow. In vitro means test tube. "The results showed that particular concentration of noni juice extracts could kill cancer cells in vitro." the scientists concluded (Fontanilla, C.D. Benefits Derived from PhilNONI. 2008).

Diallyl disulfide (the pungent element of garlic) reduces cancer initiation, promotion, and progression. S-allyl cysteine blocks the start of tumor (Kumar, N.B., Ph.D. RD, FADA, et al. Integrative Nutritional Therapies for Cancer. 2002 :49).

We have a family friend suffering from MND. She is being treated by stem cell therapy but hydroxyl radical is overwhelming her because free radicals and peroxides are not dealt with. The treatment protocol should be: reduce the population of ROS and hydroxyl radical by chelation therapy and rebuild the nerves and muscles by stem cell therapy. I suspect that she had been exposed to chlorine because her family owns a swimming pool where the water might be being treated with chlorine. Hypochlorous acid is a "brutally destructive combination of hydrogen peroxide and chlorine" (Sharma, H. Freedom from Disease. 1993:46).

Research on free radicals and ROS is now on the march. So is on eicosanoids that involve free radicals. For example, COX produces superoxide as by-product in the production of eicosanoids, thromboxane and prostacyclin that should balance each other in the body. (I have a Hub "How Some Pain Relievers (COX-2 Inhibitors) Induce Heart Attack" that elaborate on thromboxane and prostacyclin).

Adriamycin used in chemotherapy by conventional medicine produces a lot of free radicals that destroy cancer cells and inflict damage on healthy cells in the vicinity of cancer cells (Sharma, H, MD. Freedom from Disease. 1993). However, conventional medicine would not say anything about the free radicals but would administer suppressants of free radicals just the same.

Treatment and cure for tumor and cancer within the framework of the free radical theory deserve another Hub.

Resistance victimize people

It took most of those in the medical profession 40 years to adopt the germ theory of disease inaugurated by Pasteur. It was Joseph Lister who propagated the use of antiseptics which saved a lot of mothers delivering their babies, saving their babies as well. It used to be that doctors attending to mothers giving birth came straight from the morgue without applying antiseptics on their hands and other parts of the body. Mothers would die of infection owing to microbes in the dead. Carbolic acid was the antiseptic at that time,

The free radical theories of disease has been around since 1962 and most health professionals do not recognize free radicals and ROS as causes of disease. The ultimate victims are people who could contract tumor and cancer and those who are already suffering from them. The main reasons being that they are not informed of alternative methods of prevention, treatment and cure at best and are denied of effective alternatives at worst.