We all know that prevention of cancer is top priority — not just for individuals, but also from doctors’ point-of-view.
To understand the idea, we need to first begin with how cancer probably starts, or originates.
As we all know, molecular biology — which provides us with certain early-cancer clues — is focused on unravelling wayward signals that destabilise cells. On the other hand, it is epidemiology that helps us ‘zero-in’ on environmental factors — or, tangible triggers of certain forms of cancer, which are somewhat clear-cut to aim.
Epidemiology is the study of the distribution and determinants of health-related states, or events, in specified populations and their application to control health perplexities.
Strategic Crusades
Cancer prevention strategies, for long, have included crusades against smoking, sun bathing, and obesity. What has been appropriately drilled into our minds for just as long, at several levels, may not be all-pervasive, though. Smoking in public places still continues unabated in communities, despite the fact that several nations have banned smoking in public.
Passive smoking is a cancer risk, no less.
Agreed that in our battle against cancer, we now have a plethora of information — right from media-initiated reports and articles on the subject to a host of ’Net resources and websites advocating the use of diets rich in fruits and vegetables — most importantly, antioxidants. You’d think of one major, and highly celebrated, example: green tea.
Also efforts to nab the cancer bug early have expanded in their scope, thanks to technological advance. You name it, and we have access to making use of them in the best manner possible — detection screens, such as Pap smears, mammograms, and prostate specific antigen [PSA] tests. Apart from this, we also now have the benefit to bank upon pharmaceutical specialities that defy cancer just before, or as soon as it starts. This, as you know, is called chemoprevention.
But, the big question is: is this enough? The answer is a big no.
Genetic Expanse
Research reckons that an over-expressed cancer gene [oncogene] may set off an event to incite cancer in some instances — especially in family-related cancer states. This, they further observe, may also be triggered by a disabled tumour-suppressor gene — present from birth. This can again lead to cancer at any point in life.
There is also yet another ‘catch.’ You get the point. What are far more common are non-familial cancers. This is not all. In non-familial cancer states, environmentally-induced mutations may push a cell down through an alternative route to provoke cancer. This notation expands slowly as other genetic aberrations build up. When this happens, it is only a matter of time for the gene expression outlines to change. The next step is disastrous — the disease gets a firm foothold and intensifies in its development.
While it is well-known that cancer develops from environmental triggers primarily housed in the genes, it is still, however, a tall task to decipher how exactly the genes themselves interact with each other in the disease’s progression.
Today, the best environmental hazard paradigm is portrayed by the dangerous link that exists between smoking and lung cancer. In addition to this, we also now have the possibility of nutritional deficiencies facilitating the onset of cancer in certain individuals.
Preventing Cancer
Yes, it is quite possible to prevent cancer — if it is possible. Epidemiology, as touched upon earlier, is one major advance and also drawback of this idea, more so, because the incidence of cancer differs from one population to the other. Besides, the type of cancer that may affect one intensely than the other in a given population and vice versa is another pointer — and, food for thought.
In Japan, for instance, there has historically been a high incidence of gastric cancer, unlike the US, where the incidence of colon cancer is high. Today, the first generation of Japanese, in the US, have seen a dramatic change in the pattern. Clinicians suggest that this could be due to a definitive change in dietetic models too [Western diet], but not necessarily genetics. The inference? It is the environment that has brought about the change.
There is, of course, no fail-safe method, or plan, with which one can prevent cancer. One neat way of doing, perhaps, as scientists now attest, is by asking the cells in our body not to divide — which is a mammoth task. Cell division is far too complex than any other complex entity known. Medical specialists, therefore, say that it is more practical if one sticks to doing things that lower the risk of cancer — taking care of one’s health, eating a balanced diet, with several servings of vegetables and fruits, doing exercise and, most importantly, not smoking. All this is, again, no guarantee, but it is sure a doable plan of action instead of just accepting the fact that the risk of cancer is something we have to learn to live with, or expect.
Tricky Customer
Environmental exposure, or deficiency, common to some types of cancer may reveal how the disease starts, but this is not always a dependable proposition. Just like epidemiological observation. On the face of it, epidemiological data are valuable, but if one takes into consideration the several conflicting factors that truly make up data, it is confounding. Is there a better way, you may well ask. There is, says Dr Bruce Ames, PhD, Professor Emeritus Biochemistry and Molecular Biology at University of California, US. His strategy is — “Reverse the process, and look at human cells in culture, deficient in one nutrient, and see what happens.”
Well, deficiencies of vitamins B12, B6, or folic acid, are reported to replicate the DNA, ‘rip-off’ the chromosomes, and cause cancer. Nutrients, like beta-carotene, a vitamin A precursor, and an antioxidant, are said to protect against cancer; they keep cell activity intact and specialised. Selenium, a micronutrient, is said to protect against cancer. Research also evidences that vegetables rich in beta-carotene reduce the risk of cancer substantially. There are others too, such as vitamin C and E, two great nutrients, which have well established antioxidant properties.
Today, cancer research and therapy are geared to one major focus: malignancy. Although conventional drugs to prevent occurrence, or inhibit growth of a precursor lesion, is also a focus, or the basis of chemoprevention, there are several nutrients and phytochemicals [nutraceuticals] that have been found valuable for prevention. It is clear that fibre in food, for one, prevents colorectal cancer. This is based on a simple premise — fibre flushes toxic substances out of the body.
Cuing-In On Cancer Risks
One quick way to hit upon a cancer risk, according to modern research, is by way of biomarkers, not symptom picture, which is not always apparent. It may also, in addition, be possible to monitor precancerous tissues [e.g., intestinal polyps, or oral lesions] to pinpoint a cancerous invasion.
Whatever the cue for diagnosis, we are far from a point where one would be able to ‘pop a pill’ to prevent cancer. You get the point. Besides, people are also wary of taking medications — fearing side-effects.
One way of engineering chemopreventive and other medications acceptable to the discerning consumer, as clinicians attest, is by making conventional drugs relatively safe. This has more to it than what meets the eye. According to Dr Michael Sporn, MD, the Oscar M Cohn Professor of Pharmacology and Toxicology at Dartmouth Medical School, US, “People say, ‘How dare we treat healthy people with drugs that subject them to risk?’ But, how dare we not treat someone who we know has a high risk, when we have something to diminish that risk. We can identify people at high risk using genetic and proteomic [cancer] markers, and start to think about intervening earlier.”
Sceptics say that this idea carries a double-edged sword. One the one hand, it can prevent cancer and, on the other, it can lead to drug-induced problems. For example, most adenomas [benign cancer states] do not progress to cancer. Also, long-standing use of aspirin, a cancer-pharmaceutical may, for instance, result in life-threatening complications.
Also, further along the road for chemoprevention are encouraging results that have emerged from selective oestrogen receptor modulators [SERMs] in breast cancer, to highlight one example. Tamoxifen, a SERM, given to women with oestrogen receptor-positive disease has been evidenced to prevent cancer in the unaffected breast — though responses are diverse for it in medical circles.
This brings us to one important perspective — that for cancer prevention to work we need to aim at multiple levels, keeping in mind the awesome possibilities of one tumour developing over a period of time to cancer. Just one cell is all that is needed for a tumour to grow — a tumour that cannot be whisked away by natural mechanisms. You get the point. Again. It is a formidable task to stop cancer in its pathway, as it were.
The bottom line, as a result, as research says, needs to be practical and achievable. We need to slow down cancer in its tracks with newer and more potent, but less harmful, therapies — this should also include integrative medicine and complementary and alternative medicine [CAM] protocols. This is what open-minded, current research is aiming at and hoping for to happen sooner than later.
Dr RAJGOPAL NIDAMBOOR, PhD, is a wellness physician-writer-editor, independent researcher, critic, columnist, author and publisher. His published work includes hundreds of newspaper, magazine, web articles, essays, meditations, columns, and critiques on a host of subjects, eight books on natural health, two coffee table tomes and an encyclopaedic treatise on Indian philosophy. He is Chief Wellness Officer, Docco360 — a mobile health application/platform connecting patients with Ayurveda, homeopathic and Unani physicians, and nutrition therapists, among others, from the comfort of their home — and, Editor-in-Chief, ThinkWellness360.
[This article was first published March 27, 2022]
