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HyperMED - Cancer Recovery

 

 

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Cancer can affect us all - family and friends. This section is dedicated to Dr Hooper's sister (Leearne) who recently died from progressive adenocarcinoma of the stomach. Leearne's tribute 

 

Background

1971 President Richard Nixon declared 'War on Cancer'. 32-years later and approximately US $2-trillion has been spent on conventional cancer treatment and clinical research but are we really any closer to finding a cure?

Certainly any 'tax payer' would rightly think that after almost a third of a century and enormous cost; modern day bio-science would have found the answer to the nations number two cause of death. But this remains one of the greatest unsolved mysteries and unfortunately - miseries!

Cancer statistics have turned into an obscure phenomenon generating both direct and indirect causes of death. It is highly probable that the statistics associated with cancer are in fact far greater than reported owing the complexity and hopelessness by those affected.

Cancer cells survive conventional therapies because they are highly adaptable, aggressive and 'opportunistic'. Cancer cells have ability to alter their cellular composition and virtually thrive in an increasingly competitive environment and ultimately are the dominating cellular structure remaining in virtually an oxygen deficient environment.

Chemotherapy drugs have a high rate of failure because cancer cells readily adapt and mutate.

The Journal of the American Medical Association (Welch 2000) reported that the prognosis for cancer patients has not changed much since 1950. According to this study, the 5-year survival rate for most forms of cancer was the same in 1995 as they were back in 1950. The title of this study 'Are increasing 5-year survival rate evidence of success against cancer?' The answer is unfortunately; No! Welch stated that one of the reasons more cancer patients are living longer is because of the earlier diagnosis reflective of improved clinical diagnostic investigations. The authors of the study reported that the ability of medicine to effectively treat most cancers was no better that it was in the 1950's. Similar authorities confirm these clinical observations (Epstein 1992, Spotlight 1994).

This editorial (NEJM 2002) pointed out that while new chemotherapy regimens appear to be improving survival, when these same regimens are tested on a wider range of cancer patients, the results have been disappointing. In other words, oncologists at a single institution may obtain a 40% to 50% response rate in a 'tightly controlled study', but when these same chemotherapy parameters are administered in the 'real world' setting, response rates unfortunately decline to only 17% to 27%.

In fairness, the article also pointed out that certain types of cancer are responding better now to chemotherapy compared to 30 years ago. These include lymphomas (Hodgkin's, non-Hodgkin's and Burkitt's), multiple myeloma, hairy cell leukaemia, chronic lymphocytic and certain other types of leukaemia. Depending on the timing of treatment, some institutions are also seeing better results with breast and early-stage lung cancer.

 

The fastest growing type of cancer

Over the past 25 years, the incidence of esophageal cancer (of the adenocarcinoma type) has increased 350%, faster than any other malignancy in the western world (Glenn 2001).  One study showed that esophageal adenocarcinoma cases are increasing 5% to 10% each year in developed countries. Another study showed that the rate of esophageal adenocarcinoma increased eight-fold over a 20-year period in Denmark (Bytzer 1999).

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These increased rates are strongly related to gastroesophageal reflux disease (GERD). One study looked at possible risk factors and concluded that severe reflux symptoms (heartburn), male sex and obesity, may identify patients with gastroesophageal reflux disease who are at the greatest risk for the development of esophageal adenocarcinoma (Gerson 2002).

The two common forms of esophageal cancer are squamous cell carcinoma and adenocarcinoma. Risk factors for the squamous cell type of esophageal cancer include use of tobacco, moderate to heavy alcohol ingestion and infrequent consumption of raw fruits and vegetables (Bytzer 1999).

The primary risk factor for the more difficult-to-treat adenocarcinoma directly relates to those who suffer heartburn (gastroesophageal reflux). It is the adenocarcinoma type of esophageal cancer that is exponentially increasing in prevalence.

These grim statistics require greater motivation for all practitioners involved in treating cancer patients and those individual who are potential candidates. Patients are advised to follow lifestyle changes that keep bile, acids, enzymes and food in the stomach and out of the esophagus. Some of these approaches involve eating several small meals throughout the day instead of one big meal, elevating the head end of the bed six to nine inches, losing weight and avoiding eating four hours before bedtime. The long-term use of stomach acid suppressing drugs is not recommended!

In the meantime, there is some encouraging news. Two very recent studies indicate that common vitamin supplements lower esophageal adenocarcinoma risk. The first study looked at a group of German esophageal cancer cases and compared them to age-matched healthy controls. The findings showed that vitamin E, vitamin C, folic acid, beta-carotene supplements significantly reduced the risk of both adenocarcinoma and squamous cell esophageal cancers. In this study, the use of a vitamin C supplement was associated with a 66% reduction, whereas vitamin E supplementation reduced esophageal cancer risk by an astounding 87%! (Bollschweder 2002)

The second study evaluated a group of esophageal cancer cases residing in Nebraska and compared them to a control group. The findings revealed a 50% reduction in esophageal adenocarcinoma incidence in those who consumed the highest levels of vitamin A, folic acid, zinc, vitamin B2 and other nutrients (Chen 2002).

While these studies are encouraging to vitamin supplement users, they should not be used as an excuse to ignore the lifestyle changes needed to mitigate the effects of gastroesophageal reflux (GERD). The most significant risk factor for developing adenocarcinoma of the esophagus is GERD.

Other studies have also identified specific chemicals in certain food to be cancer protective: Researchers at Johns Hopkins University in Baltimore had already identified sulforaphane as a "natural cancer-preventing agent found in broccoli and other cruciferous vegetables such as cabbage and Brussels sprouts. Sulforaphane increases the number of Phase II (detoxification) enzymes needed to protect cells from damage by carcinogens. Detoxification enzymes are sort of our body's protection against internal and external compounds that can damage DNA. Elevation of these enzymes would  boost your own body's defence against carcinogens." (HealthScoutNews 2003)


What causes cancer?

All cancers are caused by gene mutations (Thompson 2002). This simple fact is obscured by the publicity given to specific agents like cigarette smoke that cause cancer by inflicting mutations to genes. Cigarette smoke like many toxic chemicals has the ability to mutate genetic expression, which can later manifest as cancer in some people. Those who quit smoking when compared to non-smokers, still have higher rates of lung cancer later in life because the body is not always able to repair the initial gene mutations inflicted by the cigarette smoke.

There are many factors involved in gene mutation including physical trauma to cellular integrity (accidents, falls etc), excessive exposure to sunlight, excessive medical x-rays and dietary carcinogens. The aging process itself results in gene mutation, which helps explain why the risk of cancer increases as we grow older.

Most people have a difficult time grasping the complexities of genes and their relationship to cancer. The New England Journal of Medicine, November 23, 2000, identified the process in the article 'Roads Leading to Breast Cancer' stating; 

  • Cancer results from the accumulation of mutations in damaged genes that regulate cellular proliferation.

Genes regulate cell proliferation. When genes become mutated, normal cell regulatory processes are disrupted. If too many genes involved in regulating cell proliferation become mutated, the cells lose control over their own growth rate. Cancer is a disease characterized by rapidly propagating cells that expand locally by invasion and systemically by metastasis.

Once one understands this basic concept, it becomes apparent that if we are to prevent cancer from developing in our bodies, every practical step must be taken to maintain gene (cellular) integrity. Gene mutations can turn healthy cells into malignant cells. As gene mutations accumulate, the risk of cancer sharply increases. What we do, eat and even think about eventually effects the progression and outcome of this process.

 

Preventing gene mutations

It is not possible to prevent all gene mutations. Fortunately, cells possess repair mechanisms that protect against most cancer-causing gene mutations (Perera 2000, Malins 2002). However if the underlying reparative capabilities are inadequate then gene mutation occur and can be 'triggered' which starts the clock rolling!

There is a limit, however, to the number of gene mutations that can be repaired. That is why avoiding second-hand cigarette smoke, unnecessary x-rays (obviously Magnetic Resonance Imaging (MRI) is the most effective form of diagnosis without the harmful effects of radiation), excess alcohol, and known dietary carcinogens is so important.

The most prevalent cause of environmental genetic mutation is the food we eat everyday. A close second is consequence that occurs as a result of trauma directly affecting the normal structural and functioning integrity. 

The prevalence of cancer continues to increase at a frightening pace, however smoking rates have declined drastically since the 1950s. We were led to believe that smoking was one of the major contributors! The increased rate of cancer points to other sources of gene mutation, with the increased consumption of the wrong kinds of foods being a prime suspect.

The National Cancer Institute has issued an exceptionally large number of press releases urging people to consume at least five servings of fresh fruits and vegetables each day (Dixon 2001, Davis 2001). Dangerous foods such as over-cooked meats and fish that are loaded with gene-mutating heterocyclic amines are abundant in processed foods which are designed for taste and convenience. Unfortunately, the list of 'gene-mutating foods' keeps growing which is part of the reason their is considerable discord regarding gene altered food technology!

Scientists have identified dozens of cancer-preventing constituents in plants including indole-3-carbinol, folic acid, bioflavonoids, lycopene, sulforaphane, lutein and another effective anti-mutagenic agent identified is chlorophyll, which is found in green vegetables. Consumption of different types and colours of fruits-vegetables reduces cancer risk; is irrefutable.

 

Reference

  1. Clegg, LX et al. Impact of reporting delay and reporting error on cancer incidence rates and trends. JNCI 2002, October 16, 94(20): 1537-45.

  2. Sharon Begley. New statistics show increase in cancer rates, cancer rates go up, not down. Wall Street Journal, October 16, 2002, B1.

  3. Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer, & Lung Cancer-Time To Move On From Chemotherapy (editorial). N.E.J.M., 2002 Jan. 10, 346(2): 92-8, 126.

  4. Welch, H.G., Schwartz, L.M., Woloshin, S. Are increasing five-year survival rates evidence of success against cancer? JAMA June 14, 2000, 283(22): 2975-78.

  5. Epstein, Samuel. After 12 years, cancer is winning. Los Angelos Times, Monday, November 30, 1992.

  6. HealthScoutNews 2003: Broccoli pills may be in our future.

  7. Chowka, Peter Barry. Why The 'War on Cancer' Isn't Working, Whole Life Times, March 1984.

  8. Billions for 'War on Cancer' Brings Scant Results, Spotlight, April 25, 1994.

  9. Glenn, T.F. Esophageal cancer. Facts, figures and screening. Gastroenterol Nurs., 2001 Nov-Dec, 24(6): 271-3.

  10. Bytzer P., et al. Adenocarcinoma of the esophagus and Barrett's esophagus: a population-based study. Am. J Gastroenterol 1999 Jan, 94(1): 86-91.

  11. Gerson L.B. Triadafilopoulos, G. Screening for esophageal adenocarcinoma. An evidence-based approach. Am J Med, 2002 Oct 15, 113(6): 499-505.

  12. Bollschweder E., et al. Vitamin intake and risk of subtypes of esophageal cancer in germany. J Cancer Res Clin Oncol, 2002 Oct 128(10): 575-80.

  13. Chen H., et al. Nutrient intakes and adenocarcinoma of the esophagus and distal stomach. Nutr Cancer 2002 42(1): 33-40.

  14. Thompson, L., Schild, D. Recombinational DNA repair and human disease. Mutation Res 2002, 509: 49-78.

  15. Haber D. Roads Leading to Breast Cancer. N.E.J.M. 2002, Nov. 23, 343(21): 1566-8.

  16. Perera F, Weinstein I B. Molecular epidemiology: recent advances and future directions. Carcinogenesis 2000 21(3): 517-24.

  17. Malins D., et al. Antioxidant-induced changes in oxidized DNA. PNAS 2002 April 30, 99(9): 5937-41.

  18. Dixon B, et al. Let the pyramid guide your food choices: capturing the total diet concept. J of Nutrition 2001, 131: 461S-472S.

  19. Davis C, et al. Past, present and future of the food guide pyramid. J Am Dietetic Assn 2001, 101(8): 881-5.

  20. Bailar JCIII, Smith EM. Progress against Cancer? N.E.J.M. 1986 314: 1226-32.