16% of Cancer Described as Avoidable! – What About The Rest?

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The research, published in Lancet Oncology and carried out at the International Agency for Research on Cancer, studied international data for 27 cancers in 184 countries in order to identify the factors which contribute to the development of the diseases. The results suggest that 16% of all cancers are a result of infections, and of that sub-set 80% occur in less developed regions.[1]

The WHO another data crunching megalith estimates that 6% of cancers in wealthy nations and 22% in low- and middle-income countries are caused by infectious agents: viruses such as HBV, HPV and hepatitis C virus (HCV), bacteria such as Helicobacter pylori and waterborne parasites.

However, the real impact on risk is: lifestyle as this affects cancer risk, too. In the past two decades as waistlines have expanded, so has the evidence linking obesity with the risk of breast, endometrial, colorectal and other cancers.

In the mid-1970s, epidemiological studies suggested that people who ate more fruits and vegetables were at lower risk of several cancers.[2] Last year, epidemiologist Tim Key based at Oxford University concluded somewhat controversially, from nearly three dozen large studies and meta-analyses from the last 20 years that “at least in relatively well-nourished Westernised populations, a general increase in total fruit and vegetable intake will not have a large impact on cancer rates”.[3]

It is possible that the intakes of fruits vegetables and their micronutrients just did not meet the biological needs of the cells to defeat abnormal cell development, as other researchers suggest a more paleothic diet that excludes processed foods as well as including fruits, vegetables and fibre offer a better solution.[4] Plus we know that certain vegetables and fruits have greater impact on prevention than others.

Is Cancer a disease of modern life?

Some scientists consider cancer to be a recent phenomenon, arguing that it was relatively rare in ancient times. Over the past century, population-based cancer incidence has increased dramatically. These higher rates are probably due to two factors: first, we are living longer; and second, our modern age has increased our exposure to cancer-causing chemicals in our environment and to radiation through X-rays, plane travel and other sources.[5]

Incidence of cancer is moving to the developed countries as weight, lifestyle and exposures increase

Can we stop cancer before it starts?

Dozens of studies suggest that preventing some cancers has become a real possibility. One way to prevent cancer is to limit exposure to acarcinogen. This approach worked for young chimney sweeps in nineteenth century England that had demonstrated a high incidence of testicular cancer. It is also clear that notsmoking cigarettes reduces lung cancer risk. Ten years after quitting, a former smoker has only about half the risk of lung cancer compared with someone who still smokes.

Changing addictive behaviours such as smoking is hard, but there may be other ways to prevent cancer. Researchers have recently developed a cancer-preventive vaccine, and others are testing nutrients that may protect against certain cancers.

Scientists are also re-examining ancient ideas about the benefit of a healthy diet by isolating beneficial nutrients and providing them in pill form. Many chemicals in foods have been shown to kill cancer cells in laboratory studies and to prevent cancer in animals. Some of the dietary components being studied are selenium, vitamin E, polyphenols (from green tea), lycopene (tomatoes), resveratrol (grapes and red wine) and omega-3 fatty acids (oily fish). These compounds work by many different mechanisms. For example, many nutrients — such as epigallocatechin gallate (EGCG) in green tea, resveratrol in red wine, and sulforaphane in broccoli — prevent cells from going through the cell cycle, which stops them dividing and giving rise to new cancer cells. In terms of individual cancers a recent research paper in the British Journal of Cancer concluded by stating: Vitamin B12 from diet may be protective against bladder cancer, whereas consuming processed meat may increase risk.[6]

How to optimise the benefits from a healthy diet

1. Remember – all vegetables are not created equal.

Phytonutrients are most often found in pungent vegetables (like onions and garlic), bitter ones (like mustard greens), or ones with acquired tastes (like mushrooms). There are also a number of fruit and vegetables that are not major sources of phytonutrients, – such as apples and potatoes, albeit that they support fibre and SCFA production. The most potent are cruciferous vegetables (those in the cabbage family), specifically broccoli and its payload of glucoraphanin — the precursor of sulforaphane.

2. Remember – all broccoli heads are not created equal.

“So, is broccoli a good way to deliver sulforaphane?” It seems the answer is absolutely no – Different heads of broccoli can vary as much as 20-fold in their content of glucoraphanin. The specific variety, growing conditions, time of year, distance of transport and other factors all affect the concentration of phytonutrients. In fact, the most consistent way to deliver glucoraphanin was to use three-day-old broccoli sprouts.[7] Adding a bit of daikon radish to the broccoli might help eliminate these differences. Daikon radish contains an enzyme, myrosinase, that catalyses the glucoraphanin conversion.

3. Remember everyone has different genes.

Eating a known amount of phytonutrient doesn’t guarantee that a predictable amount of the cancer-fighting molecule will enter the bloodstream. Differences here can be traced to variations in the genes involved in the digestive processes. For example, the glutathione S-transferase M1 gene (GSTM1) influences the speed at which the body metabolises sulforaphane and expels it in the urine. The faster it happens, the less beneficial the broccoli.

GSTM1 is best understood in terms of the genes that influence phytonutrient metabolism, but it is only part of what is a rapidly growing list. An example of why this genetic variation makes so much difference is that, people who carry two copies of a particular variant of the UGT1A1 gene actually produce about 30% to 40% less than normal of a type of phase II liver enzyme. One study has shown that people with this genotype derive more cancer-protecting benefit from eating cabbage- and carrot-family vegetables — possibly because phytonutrients in these foods boost UGT1A1 activity closer to normal.[8]

4. Remember -human microbiomes vary.
Conversion of Soy Daidzein into Cancer Preventing Agents is affected by a variety of lifestyle modifiers.

This includes an impact from their genetic and digestive components. Our bacterial genes also determine the power of phytonutrients in our diet. Our digestive tract bacteria are significantly involved in the metabolism of the phytonutrients from soy, turning one type of isoflavones into another. So depending on your intestinal bacteria, two people who eat the same amount of soy each day might receive not only different quantities of isoflavones, but also different end-products.[9],[10]

The specific bacterium/bacteria responsible for equol which some scientists believe is one of the more beneficial forms of isoflavone; around 80% to 90% of people have bacteria that produce O-desmethylangolensin, a less active molecule. Equol and O-DMA are more biologically active than their precursor daidzein an isoflavone phytoestrogen found in soy. Interestingly, substantial interindividual differences in daidzein metabolism exist; approximately 30%-50% of the human population produce equol, and approximately 80%-90% produce O-DMA.[11]

5. Remember – your age at consumption impacts on benefits.

Studies, mostly conducted on animals and epidemiology analysis of human consumption of soy, miso and tofu suggests that benefits in terms of cancer reduction is linked to early age intake. It also seems unlikely that if the individual refuses to change from a typical western diet that the impact is minimal.[12] But eating it throughout formative years does seem to reduce risk against breast cancer despite a later shift in food selection.[13]

6. Remember – phytonutrients can be difficult to extract.

The essential ingredients found in berries and other phytonutrient foods tend to be available on a seasonal basis and may be too expensive to encourage year round consumption, this may lead to inadequate intakes of the foods to impact on cell differentiation and prevention, Supplementing the diet with concentrated food supplements is considered a supportive approach, but does not confer the same whole diet benefits and must not be seen as a replacement to overall food selection, but as a key nutrient amplifier.

7. Remember – The total diet is greater than its individual parts.

It is likely that these effects are not limited to experimental concoctions. Gut bacteria influence how phytonutrients are processed, but fibre intake and other aspects of the diet alter the gut ecosystem. Selecting food groups that favour a wide range of key nutrients as well as those that favour beneficial bacterial compositions will have a greater impact on risk reduction than isolated compounds. This may also include the use of specific strain bacteria and cooperative isolates to extract the best overall benefits.[14]

References


[1] De Martel C, Ferlay J, Franceschi S, Vignat J, Bray F, Forman D, Plummer M. Global burden of cancers attributable to infections in 2008: a review and synthetic analysis. The Lancet Oncology, Early Online Publication, 9 May 2012 doi:10.1016/S1470-2045(12)70137-7 View Abstract

[2] Armstrong B, Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int J Cancer. 1975 Apr 15;15(4):617-31. View Abstract

[3] Key TJ. Fruit and vegetables and cancer risk. British Journal of Cancer (2011) 104, 6–11. doi:10.1038/sj.bjc.6606032 View Full Paper

[4] Lindeberg S. Paleolithic diets as a model for prevention and treatment of Western disease. Am J Hum Biol. 2012 Mar-Apr;24(2):110-5. doi: 10.1002/ajhb.22218. Epub 2012 Jan 19. View Abstract

[5] David AR, Zimmerman MR. Cancer: an old disease, a new disease or something in between? Nat Rev Cancer. 2010 Oct;10(10):728-33. Epub 2010 Sep 3. View Abstract

[6] J W Wu, A J Cross, D Baris, M H Ward, M R Karagas, A Johnson, M Schwenn, S Cherala, J S Colt, K P Cantor, N Rothman, D T Silverman and R Sinha Dietary intake of meat, fruits, vegetables, and selective micronutrients and risk of bladder cancer in the New England region of the United States British Journal of Cancer , (8 May 2012) | doi:10.1038/bjc.2012.187 View Abstract

[7] Fahey JW, Zhang Y, Talalay P. Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10367-72. View Full Paper

[8] Ambrosone CB, Tang L. Cruciferous vegetable intake and cancer prevention: role of nutrigenetics. Cancer Prev Res (Phila). 2009 Apr;2(4):298-300. Epub 2009 Mar 31. Review. View Full Paper

[9] Lampe JW. Is equol the key to the efficacy of soy foods? Am J Clin Nutr. 2009 May;89(5):1664S-1667S. Epub 2009 Apr 8. View Full Paper

[10] Atkinson C, Frankenfeld CL, Lampe JW. Gut bacterial metabolism of the soy isoflavone daidzein: exploring the relevance to human health. Exp Biol Med (Maywood). 2005 Mar;230(3):155-70. Review. View Full Paper

[11] Yuan JP, Wang JH, Liu X. Metabolism of dietary soy isoflavones to equol by human intestinal microflora–implications for health. Mol Nutr Food Res. 2007 Jul;51(7):765-81. Review. View Abstract

[12] Wu AH, Yu MC, Tseng CC, Pike MC. Epidemiology of soy exposures and breast cancer risk. Br J Cancer. 2008 Jan 15;98(1):9-14. Epub 2008 Jan 8. Review. View Full Paper

[13] Maskarinec G, Noh JJ. The effect of migration on cancer incidence among Japanese in Hawaii. Ethn Dis. 2004 Summer;14(3):431-9. View Abstract

[14] Maslowski KM, Vieira AT, Ng A, Kranich J, Sierro F, Yu D, Schilter HC, Rolph MS, Mackay F, Artis D, Xavier RJ, Teixeira MM, Mackay CR. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature. 2009 Oct 29;461(7268):1282-6 View Abstract

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