The Medical Science Approach
This is a very ‘dry’ blog which I thought could be useful for those people unfortunate enough to have been diagnosed with cancer, and who do not understanding the orthodox explanation of the creation of a cancer mass. I have been doing a series of blogs on aspects of cancer, for our ‘Healing from Cancer Support Program’ which we have run for more than 20 years now.
How does a cancer cell form?
Cancer is an incredibly complicated disease and it is acknowledged that, just as every person is unique, every cancer mass is unique, and can have hundreds of different mutations in its cells. Mutations denote that these cells are damaged and struggling to survive. Also, if two breast cancer specimens are compared, the set of mutated genes are never identical. However, with all these differences, scientific medicine suggest several underlying hallmarks that every cancer cell shares in its transformation from being a single healthy cell, into a cancer cell.
Scientists have isolated several anti-cancer defense mechanisms that are hard-wired into each cell to stop it from becoming cancerous. These mechanisms have to be circumvented for a cell to go through a transition from being a ‘cooperating community cell’ to behaving independently of the general community behaviour—as a cancer cell.
It must be noted that when a normal cell evolves into a cancer cell, our immune system will attempt to identify and eliminate it. The following discussion is not focused on immune system activity on eliminating cancer cells—that will be presented in another series. Rather this discussion is focused on the accepted ideas that explain how normal cells become cancerous, form cancer masses, and metastasise to distant tissue sites in the body.
Common Traits of Cancer 1.
Cancer cells don’t have the same language as normal cells
Healthy cells that make up an organ (heart,liver, kidney etc) need to communicate with each other so they can act as a community to buffer environmental changes that may threaten the survival of the organ. Much of this occurs through chemicals, known as ‘growth-factors’, which help individual cells to behave as a community. These growth-factor chemicals indicate to cells when they should feed, when they should detoxify, and the times when each cell should divide, among other things. This communication between cells is a super-complex signalling web of growth-factor chemicals activating and repressing one another to form a chemical ‘song’.
Each organ cell will not divide without being ‘told’ by the growth-factor song. Damaged cells with altered surface receptors or changes to the internal cell environment, lose the ability to interpret the songs correctly. They have difficulty synchronising with other cells, and at some point when they have real difficulty adhering to the ‘songs’, they change their behavior from community behavior to ‘doing their own thing’—in order to survive within the organ environment. They begin to secrete their own growth factors—they begin to create their own ‘song’—as they cope with the changes to the organ micro-conditions within which they find themselves. Their chemical ‘song’ has an influence on cells within their vicinity to modify their behavior to assist the newly forming cancer cell to survive and replicate independently of the organ community structure.
A cancer mass is not made only of cancer cells. Cancer masses are complex tissues in which the cancer cells have co-opted and subverted normal neighboring cells to assist them. The apparently ‘normal bystanders’, such as cells of the nearby blood vessels and connective tissue, play key roles in assisting cancer masses to grow.
Medicinal herbs have been reported to stimulate immuno-modulatory activity to disrupt cancer cell ‘songs’. These are: Garlic (Allium sativum), Licorice (Glycyrrhiza glabra), Plantain (Plantago major), and Sea buckthorn (Hippophae rhamnoides) and Gotu Kola (Centella asiatic a).
Common Traits of Cancer 2.
Cancer cells have lost the ability to synch with community cells.
The formation of a cancer mass occurs because the broader cellular community (including the immune system cells visiting the organ) has lost its influence over the replication cycles of cancer cells. Cancer cells replicate whenever they can—when there is sufficient nutrition to power their replication—rather than in sync with the overall community’s need for new cells to replace old or dying cells. What goes wrong in a cancer cell to make it independent of the community of which it was an original member? One of the reasons is due to the loss of ‘safety valves’ in the replication cycle of cells—due to metastases.
Think of a cell replication cycle being similar to the control system of a washing machine. A washing machine passes through several stages in a wash cycle; soaking the clothes; adding detergent at the correct time; rinsing the clothes for the appropriate duration to remove the detergent; adding the fabric softener at the correct time; a final rinse and then spinning the clothes to remove as much water as possible.
In much the same way, the cell replicating cycle is a series of tightly regulated events inside a cell that leads to its division from one cell into two cells. In between these ‘start and end’ states, the DNA inside the parent cell first has to double itself, and then divide equally into the two developing cells. There are feedback loops that guide the cell through replication checkpoints at every stage. These checkpoints act as ‘safety valves’ to ensure that an incorrectly dividing cell with damaged DNA, is able to be destroyed rather than allow it to continue its development into a damaged cell—a cancer cell.
A cell replication cycle has four stages.
Stage 1. The cell actively grows in size, and prepares the chemicals for DNA synthesis. At the end of this stage, there is the first checkpoint as the cell monitors its environment, to make sure there aren’t any ‘stop’ signals. If okay, DNA replication takes place. If there is damage to the DNA, the checkpoint prevents further replication. Each checkpoint is made up of regulatory proteins (called cyclins and cyclin-dependent-kineses) that are like growth-factors, except that they inhibit growth rather than promote growth.
Stage 2. The cell continues to grow after DNA replication, and when large enough, a second checkpoint determines if the completed replication of DNA is error-free. If it is damaged, the replication stops and the cell dissolves the new DNA.
Stage 3. This is called mitosis. The cell growth is complete and the cell goes through division into two equal ‘daughter’ cells.
Stage 4. At any stage, cells can be forced into a resting stage and stop replicating—if the environmental conditions are not right. They can also resume replication when the conditions are right. When cells totally mature, they generally stop replicating permanently.
Thus, each cell has three choices: it can grow and divide by staying in the first three cell cycle stages; or it can take a temporary break by entering a resting stage (Stage 4.); or it can permanently exit the cell replication-cycle into the mature state. The checkpoint proteins are responsible for stopping cell replication by directing the cell into either the resting stage, or the mature state.
For a cancer cell to continue to divide, it is not able to respond to the checkpoint signals. Nearly all checkpoint chemical ‘mechanisms’ are linked to a tumour-suppressor-protein in the DNA, known as the retinoblastoma-protein (discovered in 1971). This protein acts as the main ‘brake’ in the cell cycle progression, when it monitors ‘yes’ or ‘no’ signals from the organ community to allow replication. The majority of human cancer cells have ‘mutation-induced defects’ in the retinoblastoma-hand brake, and this stops the check-point from acting efficiently to stop further replication. Thus cancer cells can continue replication independent of the community ‘instructions’.
The alkaloids in the medicinal herb Periwinkle (Catharanthus roseus) have been successfully used in the treatment of various cancers such as Leukemia, Hodgkin’s disease, Malignant lymphomas, Neuroblastoma, Wilm’s tumours, Kaposi’s sarcomas, Mycosis fungoides. The action appears to be related to focused assistance of retinoblastoma-protein function, to prevent cells forming into cancer cells.
Common Traits of Cancer 3.
Cancer cells evade apoptosis (cellular suicide)
Apoptosis is a term that means the opposite of cell growth—it means ‘cell death’. To divide and grow uncontrollably, a cancer cell not only has to not-respond to normal cellular-replication ‘checkpoints’, but also it must evade the cellular-death triggering mechanism. Indeed, this acquired resistance to cell death is characteristic of all types of cancers.
The apoptosis programming is hard-wired into every cell in our body. It is like a cyanide capsule, which quickly delivers death, if the circumstances require the cell to ‘commit suicide’. If a normal cell detects that its DNA has become damaged, it has the option (among others) to trigger apoptosis and thus remove itself from the community population of organ cells. Apoptosis, is an entirely normal function of community cells. A similar apoptosis response is activated when a tadpole changes into a frog—the cells in the tail die through apoptosis, and the tail disappears. Apoptosis is a tidy process in which the cellular walls break down; the chromosomes degrade; the DNA breaks up into fragments; and the dying, shrinking cell is then swallowed up by neighboring cells or a patrolling immune cell.
So how does apoptosis work? The ‘machinery’ of apoptosis is responsible for monitoring both the interior and exterior environments of the cell for conditions of abnormality, in order to decide whether that cell should live or die. These abnormalities are such things as; DNA damage, signalling irregularities, lack of available oxygen, lack of available nutrition, toxicity, etc.
The suicide machines of the cell—are called caspases
The control for apoptosis is located in the mitochondria of a cell. Mitochondria are tiny organelles floating in a cell which function as the cell’s energy factories. They contain a signalling molecule known as cytochrome-c, which is bound to the mitochondrial wall. In response to the signals to commit suicide, the mitochondria release cytochrome-c molecules, which form into proteins known as caspases—which then degrades the cell in apoptosis.
The repairers of the cell DNA—are called P53 genes
The P53 gene is a repairer-gene, and it is used to maintain the integrity of the DNA structure of the cell. More than half of all cancers have inactive P53 gene defects. When activated by either DNA damage or chromosome abnormalities, the P53 gene can stop the cell cycle and initiate DNA repair. If repair is successful, the cell cycle is restarted. If repair is not successful because the damage is too great, then the P53 gene facilitates cell apoptosis. Cancer cells have defects in P53 genes
So how do cancer cells overcome the P53 gene from monitoring damage to their DNA that will cause them to stop the cell replication-cycle and initiate apoptosis? The most common reason appears to be the actual loss of the P53 gene due to DNA mutations and/or viral activity. It is no surprise that the highly aggressive cancers often have defects in both retinoblastoma and P53 genes. As a result, these rapidly growing cancers have extremely low levels of apoptosis and extremely high levels of cell division.
Medicinal compounds from herbs and concentrated derivatives from some of the plants that humans eat, are being connected with improvements in anti-oncogene performance, particularly P53. These include curcumin from turmeric; genistein from soybean; tea polyphenols from green tea; resveratrol from grapes; sulforaphane from broccoli; isothiocyanates from cruciferous vegetables; silymarin from milk thistle; diallylsulfide from garlic; lycopene from tomato; rosmarinic acid from rosemary; apigenin from parsley and gingerol from gingers (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4017674/).
Common Traits of Cancer 4.
Cancer cells evade the Cellular Timekeepers
Normal cells are hard wired with a timer that keeps track of their age as well as the number of times they divide and grow. Most cells in our body will only undergo a limited number of successive cell growth-and-division cycles. This limit has been named the ‘Hayflick Limit’ after its discoverer, Leonard Hayflick. After undergoing between 40 to 60 divisions, cell growth slows down and eventually stops altogether. At this final stage it is known as senescence, and it is irreversible. The cell does not grow or divide anymore, but can remain alive.
When normal human cells are cultured in a petri dish, almost all the cells grow and divide a set number of times, and then enter senescence. A tiny number of cells go beyond the senescence stage and continue to divide for a little while. However these cells eventually undergo another phenomenon known as ‘crisis’, in which the ends of their chromosomes fuse with each other, and the population of cells created since senescence, die on a massive scale due to apoptosis.
How does a cell ‘count’ the number of times it divides, and ‘know’ when to stop? The answer is telomeres. Telomeres are regions of DNA that cap and protect the ends of the chromosome from degrading or from fusing with another chromosome. Without telomeres, each time a cell divides our genomes would progressively lose information—because the chromosomes would get shorter and shorter. A telomere is like the heat-shield of a spacecraft; it protects the actual spacecraft and absorbs the damage instead of the spacecraft. With every replication of a cell, between 50 to 100 nucleotides of telomeric DNA are lost. This progressive loss eventually causes the telomeres to lose their ability to protect the ends of chromosomes. Left unprotected, these exposed ends become damaged, and at some point, a DNA damage response is activated to stop further growth—this is the senescence stage. There is the possibility that when the telomeres erode and the chromosome ends are exposed, they can fuse with each other. This produces irreversible DNA damage, and results in apoptosis—the cell dies.
Cancer cells repair their telomere structure
The defining feature of cancer cells is their ability to divide endlessly, without exhaustion, generation after generation. They achieve this by destroying the cellular timekeepers—the telomeres.
When cells are grown in petri dishes in the lab, repeated cycles of cell division lead first to senescence, and then if they survive, they move onto the ‘crisis phase’ and die. In very rare cases (about 1 in 10 million) a cell moves past the ‘crisis phase’ into an immortalised phase in which they can divide endlessly.
Cancer cells not only over-ride their growth limiting program linked to the signals from their internal and external environments, they also are able to breach the in-built telomere replication limit that is ‘hard-wired’ into the cell. How do they achieve this? All cancer cells maintain their telomeres. About ninety percent of them do so by increasing the production of an enzyme known as telomerase. As its name implies, telomerase functions by continually adding telomeric DNA to the ends of chromosomes. Apart from foetus cells and stem cells, most normal cells have low telomerase activity. Scientists have found that a mutation in the region of the ‘TERT’ gene for producing telomerase, makes this gene hyperactive, and the length of the telomeres are extended much more than what is considered normal. A mutation like this will allow the cell to keep replicating.
Living a long life appears to come at a price for some people. The accumulation of DNA damage to certain cells of the body increases with time—which is why cancer is basically a disease of an ageing population. It is known that DNA integrity and telomere length is affected by oxidative stress due to free radicals, and this gets worse with increased age. While this damage can be repaired in the DNA by various repair mechanisms, the repairs appear to be less effective on telomeric DNA. Telomere damage appears to be more susceptible to increases in oxidative stress, than it is to the activity of DNA replication.
Oxidative stress is an imbalance between the production of an ‘oxygen containing molecule’ that has one or more unpaired electrons (known as free radicals) and the ability of the body to counteract or detoxify their harmful effects through neutralisation using antioxidants. Oxidative stress is connected mostly with being overweight, having lack of exercise and in the eating lifestyle of people, in which toxic chemical compounds and pollutants enter the body, predominantly through diet and drink.
The main culprits appear to be related to individual reactions to plant foods that we consume. Grain gluten and agglutinans are the worst offenders. Others are hydrogenated oils from plants that are cooked at higher temperatures; cigarette smoke; table sugar, high fructose corn syrup and fructose in fruits and some vegetables; food preservatives, coloring’s and flavorings; various prescribed drugs; plastics; and petrochemicals in general.
The herbs that are most likely to assist with telomerase production stability, are Astragalus root, and Milk Thistle. Other medicinal herbs which can be used in conjunction with these are: Pau d’Arco, Thyme, Echinacea Root/leaf, and Cloves. Foods that are also being linked to telomerase production stability are eggs and saturated animal fats.
Common Traits of Cancer 5.
In a developing embryo or a wound that is healing, the communities of cells are organised by the immune system to undertake specialized tasks beyond the ability of any single cell, such as the complexity associated with tissue formation. These cells are also supplied with oxygen and nutrients by the immune system, which also organises the removal of metabolic wastes. Under direction the immune system, these cells also form tissues for new blood vessels in a process known as angiogenesis. This assists the supply of oxygen and nutrition into the growing tissue, as well as the removal of cellular metabolites due to cell respiration, from the growing tissue. In a similar manner, a growing cancer mass also requires more and more access to nutrients as well as waste disposal (cancer cells do not need oxygen, they obtain energy through fermentation).
Nutrition in the form of glucose can be obtained by cancer cells mostly through intra-cellular diffusion, but beyond about 1mm in diameter, the movement of glucose through a cancer mass is generally insufficient to supply those cells at the center of the mass with sufficient nutrition to survive, so these cells begin to starve. In response to this, these cancer cells send out signals, to the healthy cells of nearby blood vessels, that there is a need for tissue growth to supply glucose to the starving cells.
A complex interaction then occurs between healthy cells and the immune system, for this process to proceed. If this subterfuge works, then tissue is directed to grow from an artery, to form a supply pipe to carry glucose linked to the blood, directly into the center of the cancer mass. Thus, cancer cells subvert these healthy neighboring cells into playing a key role in allowing the cancer mass to survive and develop. Angiogenesis in a cancer is a perversion of a normal cellular process, a perversion that is an essential requirement for the development of cancer masses of any size above 1mm in diameter.
Many experiments show that there are certain chemicals which can block angiogenesis and impair the growth of tumours. While ‘Avastin’ was the first commercially available angiogenesis inhibitor, there are natural medicinal herbs that also do this job without the side effects of ‘Avastin’. The herbs that are traditionally used for anti-cancer treatment, and that are anti-angiogenic through multiple interdependent processes (including effects on gene expression, signal processing, and enzyme activities) include Artemisia annua (Chinese wormwood), Viscum album (European mistletoe), Curcuma longa (curcumin), Scutellaria baicalensis (Chinese skullcap), resveratrol and proanthocyanidin (grape seed extract), Magnolia officinalis (Chinese magnolia tree), Camellia sinensis (green tea), Ginkgo biloba, quercetin, Poria cocos, Zingiber officinalis (ginger), Panax ginseng, Rabdosia rubescens hora (Rabdosia). (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891180/).
Common Traits of Cancer 6.
Tissue Invasion and Metastasis
If a cancer mass keeps growing it must eventually spawn ‘pioneer cells’ which move out of the original mass to invade adjacent tissues as well as travel to distant sites where they can grow into new masses—which are called metastases. With the exception of the leukemias and some brain tumors, metastases cause the majority of cancer deaths.
When cancer cells move away from an original site of growth in an organ, they either migrate through the blood stream or through the lymph system. The immune system will destroy most of these free-travelling cancer cells while they move through these channels. But what allows a new mass of cancer cells to grow at a distant site and not be mopped up by the immune system?
In biology theory, our bodies have a blueprint to create our physical body—this basis is in the DNA of our differentiated cells originating from ovum and sperm DNA. Our immune system regulates our cells to adhere to community DNA construction—organ tissue structures. Individual cells tether themselves to one another to form tissues that perform a specific functions. Tissues form as organs and organs combine to form our bodies.
Our tissues are composed primarily of two types of cells—epithelial and mesenchymal cells. Epithelial cells adhere to one another to form cell layers, which act as barriers to isolate our bodies and organs from the environment and mesenchymal cells are solitary and capable of migrating. Our body is not made up solely of cells. A large proportion of our body consists of extracellular space, which is filled with a mixture of carbohydrate, fat and protein molecules. This space is known as the extracellular matrix.
Several classes of proteins are involved in the tethering of cells to their surroundings. Immunoglobulins and cadherins mediate cell-to-cell adhesion’s while integrins link cells to the extracellular matrix. All of these interactions convey regulatory signals to the cell and should not be viewed as static connections that simply hold cells in place. The most important protein cementing cells to each other is known as E-cadherin. The coupling of cells by E-cadherin results in the transmission of anti-growth signals. This is one of the mechanisms of a phenomenon known as ‘contact-inhibition’, where cells that touch one another do not grow any further. Metastasis therefore requires the un-tethering of these bonds, to allow types of cancer cells to migrate freely. Not surprisingly, E-cadherin function is lost in migrating cancer cells. Conversely, another molecule known as N-cadherin shows increased levels in migrating cancer cells, as this molecule helps the cancer cell to slip through blood vessels during migration.
Migrating cancer cells change their appearance, from a somewhat, variable cobblestone-like shape, to being spindly. The cells also un-tether themselves from the extracellular matrix. They stop expressing E-cadherin, so that the cement that binds them to other cells is eliminated. They express more N-cadherin, so they can move through blood vessels to distant sites more efficiently. A metastatic cancer cell has increased motility and is resistant to apoptosis.
Metastasis and invasion are complicated processes. For example, macrophages, one type of immune cell, appear to be easily exploited by cancer cells to contribute to cancer migration. These cells are attracted to the edges of the tumor and supply it with enzymes to enable the cancer cells to break free of surrounding tissue and begin the process of migration. These subverted macrophages can also supply growth factors to cancer cells under certain conditions, to enable them to continue to divide and proliferate. Cancer cells stimulate the macrophages by producing a chemical they require called ‘Essential Growth Factor’—also known as ‘Colony-Stimulating-Factor’.
Metastasis has been traditionally thought of as the final stage of cancer, once a cancer mass had grown to a size which forces newly growing cancer cells ‘out of the nest’, for want of enough space to continue to grow. Recent evidence now suggests that metastasis does not necessarily happen in the final stages of cancer progression, but can occur at any time in the growth of a cancer mass—even before a primary cancer can be detected with conventional equipment. The ability to invade and metastasise distant sites is a signature of cancer cell aggression.
The following herbs (in combination) have been used in Chinese medicine to stop metastasis: Cordyceps fungus (Cordyceps sinensis), White flower snake-tongue grass (Hedyotis diffusa), Qing dai (Indigo pulverata levis), Butt rot fungi (Polyporus umbellatus), Astragalus (Astragalus propinquus), Ginseng (Panax ginseng), Black nightshade (Solanum nigrum), Patchouli (Pogostemon cablin), Black atractylodes rhizome (Atractylodis macrocephalae rhizoma), Chinese cucumber (Trichosanthes radix), Clematis (Clematis radix), Broad leaf privet (Ligustrum lucidum), and Chinese liquorice (Glycyrrhiza radix). (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880989/)
Common Traits of Cancer 7.
DNA mutations may assist cancer cells
In the same way that normal cells have to adapt to environmental changes in the body, cancer cells also have to cope with these challenges, and more. A cancer cell has to compete with other cancer cells as well as normal cells for resources; evade attack by immune cells; cope with their internal self-destruct mechanisms; take advantage of unfortunate circumstances of healthy normal cells to exploit their behavior to their own advantage; and adapt to the extra challenges encountered when migrating to other areas of the body (metastases).
There are over one hundred million-billion cell divisions occurring throughout the average human life-span. It is estimated that each of our genes is prone to several hundred million mutations during this time (each gene has about 1,700 nucleotides and each nucleotide has about a one-in-several-hundred-billion chance of being mis-copied). Most mutations are repaired in healthy cells. Typically, this repair involves cutting out and re-synthesizing damaged portions of the DNA. There are several different ways the DNA repairs itself, and these repair processes are so important for a species survival, that these repair-proteins are found in every life-form, from bacteria to our own cells.
Of course there are occasions when mutations cannot be corrected. An important question is whether mutations can be beneficial for a cell or not, to enhance its quality of survival. To propose and argue that mutations, even in tandem with ‘natural selection’, are the basis for the successful survival of the 6,000,000 species of life-forms on this planet, is not really logical, and it also goes against the fundamentals of mathematical probability. Mutations have a very limited ‘constructive capacity’ and they also occur incoherently. They are not complementary to one another, nor are they cumulative in successive generations toward a given direction. They modify what preexists, but they do so in disorder. As soon as some disorder, even slight, appears in an organized life-form, sickness then death follow.
To accept that a mutation would produce a super-viable cancer cell, capable of more efficiently adapting to the human environment than normal cells that have helped create their own body environment, is somewhat equivalent to believing in miracles. It is almost impossible for a mutation alone in a cancer cell to enable it to grow faster, or survive longer and produce more offspring than the surrounding normal cells, without other factors being involved.
However without any other major understanding of the forces causing cancer evolution, science has to keep its focus on mutations as the transitive ’cause’ of cancer formation. So most scientists accept that mutations enable cancer cells to embark on their uncontrolled growth within our bodies through changes to Telomeres, Apoptosis programming, gate-keeper control, and Retinoblastoma-hand brake mechanisms through mutations. But what if there were other factors that set conditions for alterations in DNA to be of temporary benefit?
The ‘behavior-regulators’ of DNA may be responding to emotional stress
One point five percent of the DNA material in human chromosomes is called ‘protein-coding’ DNA and it composes our genes. 98.5 percent of our DNA is called ‘non-protein-coding’ DNA, and this resides outside our genes. The protein-coding gene regions contain the information necessary for a cell to make proteins for its physical construction. Non-protein-coding regions are not related directly to making proteins, but essentially are involved with all levels of internal behavior within cells, and they regulate how much of a particular gene is expressed at any time—that is, the non-protein-coding DNA dictates whether a gene is to be switched ‘on’ or ‘off’. This type of DNA has opened many new fields of scientific research which comes under the banner of behavioral epigenetics.
Several forms of non-protein-coding DNA sequences have been isolated (Noncoding functional-RNA; Cis- and Trans-regulatory elements; Introns; Pseudogenes; Repeat-sequences; Transposons; Viral elements; and telomeres). For example, Noncoding functional-RNAs are predicted to control the translational activity of approximately 30% of all protein-coding genes in mammals and are suggested to be vital components in the progression of various diseases including cancers and the immune system responses to infection.
Mutations can occur in the non-protein coding DNA, which affect the binding of activators or repressors, chromatin state, nucleosome positioning, and also looping contacts of promoters with distal regulatory elements. This results in aberrant gene behavior which causes decay and mostly death of a cell. However there is much speculation that non-protein coding DNA responds to changes to both internal cellular environments as well as external environments, within which the cell resides—the organs and regions of the body.
According to new insights of behavioral epigenetics, traumatic experiences in our past, or in our recent ancestors’ past, leave ‘molecular scars’ adhering to our non-protein-coding DNA, which can activate under similar stressed conditions—read this as emotional stressed conditions. It seems likely that intense and prolonged emotional stress that we feel in parts of our body, may affect non-protein-coding DNA, and this may cause, Telomere, P53, Apoptosis programming, gate-keeper control, and retinoblastoma-hand brake mechanisms to dysfunction.
The Oriental scientists’ view, that emotions contribute to cancer formation, differs from that adopted by Western scientists, who regard cancer as a change in DNA that is induced by a chemical agent, radiation exposure, or insertion of viral genes, and in a few cases, abnormal DNA which is present in the genetic heritage of the individual. The cycle of progression from a healthy cell to a cancer cell is believed to occur through a series of steps (mentioned earlier), combined with the loss of the ability of the immune system to consistently destroy cancer cells at a certain rate.
Thus the cancer initiating factors act within the physical environment of the individual, combined with the person’s genetic background and nutritional status. Thus, lung cancer is mostly caused by breathing carcinogens such as in cigarette smoke; stomach and colon cancer are mostly caused by carcinogens in the food supply; skin cancer may be induced by excessive exposure to the ultraviolet light of the sun; and leukemia may be induced by exposure to industrial chemicals, radiation, or a virus that resides in the bone marrow.
Traditional Chinese doctors have been aware of these types of aetiology for thousands of years. For example, they had recognized that cancer occurs more often in certain places, and the cause was attributed to things such as the drinking water; or that cancer occur from constantly eating rotten foods and, in modern times, by smoking. Yet, it has always been the emotions that have been regarded as the most significant factor.
Excessive emotional stress and/or suppressing emotions, is thought to cause disruptions to the flow of ‘qi and blood’ through the organs, and this leads to cancer—which is exacerbated by the external environmental factors due to lifestyle.
For several reasons, Western researchers have not undertaken any detailed study of the possibility that persistent or repeated experience or suppression of emotions contributes to the risk of cancer. Aside from a low motivation to undertake the study, because other factors are considered more important, this type of research is extremely difficult to perform properly. One would have to recruit a very large number of people into the study, have some reliable method of measuring emotional status over a long period of time, and then find some way to quantify the emotional condition over time.
However, the field of psychoneuroimmunology (the study of how psychological states, as detected in activity of the nervous system, impact the immune system), has developed some evaluations that do suggest that emotional stress strongly increases a person’s susceptibility to cancer.
In China, one published study (Fan RL, et al, ‘A Study on the relationship between lung cancer at a preclinical stage and psycho-social factors: a case control study’ in The Chinese Journal of Blood Diseases, 1997; 18: 289-292.), involved 750,000 people in Beijing, where an attempt was made to determine if psycho-social factors contributed to the incidence of primary lung cancer. Their study reported three factors correlating with lung cancer occurrence:
• A period of emotional stress that appeared out of control.
• Poor working relationships between co-workers.
• Extended periods of depression.
Indeed, it is thought possible that even a single period of intense stress lasting a few months, such as occurs with a divorce, death of a family member, loss of job, or other life-changing events, is likely to lead to serious damage to tissues in specific parts of the body, which could be part of the process of the development of cancer. Stress hormones might themselves stimulate latent cancer cells into reproduction; or the hormones or their metabolites might transform a normal cell to a cancer cell; or the damage to the tissues may lead to failure of normal cancer-control mechanisms.
It is possible that emotional stress is the hidden factor, and that types of emotional stress allows mutations to occur more often in the cells of organs in specific regions of the body.
There are innumerable cases where cancer occurs after a severely stressful life event, and although these are considered as anecdotal, these phenomena do support the assertion made by traditional Chinese medicine practitioners: ‘that emotions are a major causal link in the formation of cancer, and the inability to heal from cancer’.
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