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Cancer's missing link: How bugs could be the real cause

MagazineDecember 2010 (Vol. 21 Issue 9)Cancer's missing link: How bugs could be the real cause

According to the theory, it's not a bug that we catch when we have cancer; the disease is part of a process that begins when the body's own benign bacteria begin a deadly cycle of transformation, triggered by 'carcinogens' such as smoking, pollution and radiation

According to the theory, it's not a bug that we catch when we have cancer; the disease is part of a process that begins when
the body's own benign bacteria begin a deadly cycle of transformation, triggered by 'carcinogens' such as smoking, pollution and radiation.

However, the 'cancer-bug' theorists go even further: they believe that pharmaceutical drugs-especially penicillin-can actually trigger the bacterial cycle that leads to cancer.

This extraordinary hypothesis echoes one of the first theories about cancer, one that was rejected nearly a hundred years ago. But, if the cancer-bug theory proves to be correct-that cancer does indeed start out as an infection-then medicine has been badly wrong about cancer and the best ways to treat it.

Medicine accepts that some bugs can cause some cancers. Helicobacter pylori bacteria can cause stomach cancer, and the hepatitis B virus is responsible for around half of all liver cancers. Yet, despite these 'exceptions to the rule', Henry Pitot, a professor of oncology at the University of Wisconsin, summarizes the current orthodoxy when he states that "there is no evidence that bacteria, besides H. pylori, contribute to the develop-ment of human cancer in any significant way" (J Natl Cancer Inst, 2000; 92: 1713). This position was established as long ago as 1919 by American pathologist James Ewing-who, ironically, died of cancer in 1943-when he dismissed the then-burgeon-ing theory of a cancer bug.

Today, oncologists agree that the hundred or so types of cancer are caused by a variety of factors-ranging from smoking, diet, stress and lifestyle influences to sunshine, age and genetics-that cause damage to our DNA and the natural life cycle of cells. The result is that, instead of dying, the cells continue to divide and reproduce until they create a tumour. Chemotherapy, radiotherapy and surgery are then used to attack, kill or remove the tumour.

However, over the past few years, evidence has been emerging to suggest that bacteria are playing a central role in the development of cancer, and may even be a major cause of the condition. The editors of Cancer Prevention Research, the research-based journal of the Ameri-can Association for Cancer Research, have concluded that "microbes are important causes of human cancers, and our estimation of their signifi-cance continues to grow as cancer biology is better dissected" (Cancer Prev Res, 2008; 1: 15-20, online).

The cancer-bug theory, therefore, suggests that there's a missing link in the current scientific model of cancer. Researchers at the University of North Carolina believe that the 100 trillion bacterial organisms that normally reside benignly-mainly in our gut-can become hostile as a result of poor diet, for example. In fact, they cite this as a major cause of colorectal cancer (Cancer Prev Res, 2008; 1 [7 Suppl]: CN15-02; doi: 10.1158/1940-6207.PREV-08-CN15-02).

If their hypothesis is right, it suggests that bacteria are the cause of all cancers that are triggered by 'insults'-from the diet, from taking pharmaceutical drugs, from our lifestyle and/or from the environment. According to this cancer model, smoking, for example, would not be a direct cause of cancer, but would be the trigger that transforms our usually 'friendly' bacteria into malign pathogens that can bring about inflammation, and which eventually damage both our DNA and the natural life cycle of cells in the body.

The evidence builds

Researchers are now beginning to find examples of cancers that are either being triggered by bacteria or in which bacteria are playing a significant role. Last year, researchers at the Johns Hopkins University in Baltimore, MD, discovered that a commonly found species of bacteria living in the human intestinal tract-Bacteroides fragilis-causes colon cancer. As lead researcher Cynthia Sears said, "This could be the H. pylori of colon cancer." In an experiment with laboratory mice, the researchers discovered that the bacteria cause chronic inflammation that, in turn, damages genetic material in the colon cells, allowing them to grow uncon-trollably and to develop into tumours. The bacteria have been detected in the gut of up to 35 per cent of children and adults, and in 40 per cent of patients with colon cancer
(Nat Med, 2009; 15: 1016-22).

A team of scientists at the University of Utah has identified the role that inflammation-caused, in part, by bacteria-plays in the development of cancer cells, although they see it as one of a three-part pathway that also includes hormones and what they describe as 'energy-related factors' (Cancer Prev Res, 2009;
2: 922-30; doi:10.1158/1940-6207.CAPR-08-0191).

In the UK, researchers at the University of Leicester have also reported the key role that inflamma-tion plays in the development of cancer, a process that begins with an infection that appears to cause the immune system to overreact and to protect cancer cells (Br J Cancer, 2001; 85: 473-83). These findings have been confirmed by researchers at the Cork Cancer Research Centre in Ireland, who have found that certain bacteria do indeed play a key role in the development of cancer (Mol Ther, 2010; April 13; doi:10.1038/ mt.2010.59).

In addition, other new research supporting a link between infection and cancer was presented at the American Association for Cancer Research (AACR) 101st Annual Meeting, held in Washington, DC, in April, including the following.

o A new type of lymphoma has been reported in AIDS patients. Researchers from the University of California at San Francisco say they have seen such an AIDS-related lymphoma (ARL) in more than half of all AIDS patients-and this is a cancer sub-set that is related to infection.

o AIDS patients are 100 times more likely to develop non-Hodgkin's lymphoma, and researchers at the US National Cancer Institute speculate that the risk is increased by higher levels of cytokines-proteins that are associated with infection and inflammation.

o Colon cancer risk is greater in people with increased levels of C-reactive protein (CRP), a marker of systemic inflammation. CRP is a protein found in the blood, and its levels rise in response to inflam-mation throughout the body, says Gong Yang, research associate professor at Vanderbilt University in Nashville, TN. In one study, Yang discovered that 209 of the 338 cases of colorectal cancer had elevated CRP levels, suggesting a 2.5-times greater risk.

On reviewing all the current evidence, William G. Nelson, professor of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, concluded: "Chronic or recurrent inflammatory conditions appear to contribute to the develop-ment of a diverse array of cancers, and tackling these conditions early could be an avenue for prevention" (Proceedings of the American Association for Cancer Research 101st Annual Meeting, Washington, DC, April 20, 2010).

Now you see them . . .

AIDS (acquired immunodeficiency syndrome) was first recognized as a potential epidemic in 1981, when young homosexual men began developing Kaposi's sarcoma (KS), which is caused by a virus. KS is the most commonly found tumour in AIDS patients, so much so that it's one of the key markers of a positive AIDS diagnosis.

Scientists at the AACR 101st Annual Meeting had been pondering upon the connection between cancer and AIDS, and why the two appear to go hand-in-hand. Retired dermatol-ogist Alan Cantwell had also witnessed similarities between the viruses that cause tuberculosis (TB) and cancer, and has controversially proposed that the two diseases are manifestations of one bacterial process (Cantwell AR Jr. The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. Los Angeles, CA: Aries Rising Press, 1990). He also believes that the same is true of cancer and AIDS patients.

However, for this hypothesis to be feasible, bacteria would have to be able to change-a phenomenon that biologists call 'pleomorphism'-whereas the orthodox view in biology is that bacteria are monomorphic, a theory that postulates that, aside from minor variations, each bacterial cell does not alter its features from that of its original genesis from a previous cell of specific size and shape.

In fact, Milton Wainwright, a microbiologist at Sheffield University, points out that this prevailing view is still regularly confounded by bacterial specimens taken from tumours. Such bacteria appear to be "highly pleomorphic", says Wainwright, and they pass through a complex life cycle, changing from micrococci, bacilli, fungi and, possibly, to viruses (Perspect Biol Med, 1997; 40: 407-14).

In simpler terms, the bacterium takes on a series of different life forms-somewhat like the creature in the sci-fi horror movie Alien-that allows it to shift from virus to bacterium to fungus. During this astonishing chain of metamorphoses, the microorganism also changes its size and shape. This means that it's invisible while in its viral form, and becomes detectable under the micro-scope only when it's in its bacterial and fungal phases.

The theory of pleomorphic cancer bacteria is routinely dismissed by the scientific orthodoxy as being merely a misreading of contaminated labora-tory samples, but it's a theory that cannot be explained away quite so easily. Biologists are consistently isolating a specific type of pleo-morphic microorganism-in both animal and human cancer cells-that has been described by them as "an unclassified mystery" (Ann NY Acad Sci, 1970; 174: 636-54), while a form of cancer caused by the Rous sarcoma virus is suspected of being the manifestation of just one stage in the microorganism's life cycle (Med Hypoth, 1990; 32: 1-9).
Indeed, biochemist Florence Seibert, one of the world's most celebrated scientists-who pioneered the skin test for TB that is still used to this day-has demonstrated that bacteria in cancer cells aren't the result of laboratory contamination. In a series of experiments, she was able to isolate bacteria from every tumour sample, and every blood sample from cases of acute leukaemia, that she examined (Trans NY Acad Sci, 1972; 34: 504-33). However, after making these discoveries, funds from supporters such as the American Cancer Society suddenly dried up, and Seibert was forced to put a stop to her research programme.

The idea of an 'Alien'-like bug is not restricted to cancer and other chronic diseases. Researchers have discovered that the intestinal parasite Giardia lamblia, which is responsible for millions of cases of diarrhoea every year, has protein coats that it can change in moments to throw the body's immune cells off track. Researcher Hugo Lujan, of the Catholic University of Cordoba in Argentina, has studied the parasite for many years and has discovered that it changes its cover from among 200 different protein coats in a process known as 'RNA interference' (Nat Med, 2010; 16: 551-7; doi: 10.1038/nm.2141).

Further down the microscope

There's a further twist to the pleomorphic cancer-bacteria theory. In the process of transforming, the bacteria appear to lose their cell walls, becoming what is called 'L-form' or 'cell-wall deficient' (CWD). Indeed, over the past century, researchers have identified more than 50 different species of bacteria that are capable of becoming L-form. Researchers at the Royal Brompton Hospital in London have postulated that L-forms have been associated with many chronic diseases, including cancer, and that their bizarre life cycle is triggered by an outside agency, such as an antibiotic (J Int Med Res, 2005; 33: 1-20).
If this is so, then this also feeds into the cancer-bug theory that 'friendly' bacteria can become malign as the result of an outside 'insult' such as diet, smoking and, of course, pharma-ceutical drugs.

L-form bacteria have been found on the scene of the crime in many cancer cases. In the 1980s, Emil Wirostko, a clinical ophthalmologist at Columbia University in New York, discovered L-forms in the white blood cells of cancer patients (Br J Ophthalmol, 1989; 73: 865-70), whereas dermatologist Alan Cantwell used an acid-fast staining technique to reveal L-forms in tissue samples taken from the bodies of patients who had died of Hodgkin's disease (Arch Dermatol, 1984; 120: 401-2) and other cancers (Int J Dermatol, 1982; 21: 99-106).

Researcher Lida Mattman, a senior bacteriologist at the University of Massachusetts who went on to head up a laboratory that evaluated speci-mens sent for identification from doctors, took L-form research to a new level. Not only did she confirm Dienes' findings (see box below) that L-forms can change size and shape but, more remarkable still, she also discovered that 85 per cent of TB cases had a proliferation of L-forms in the blood (Mattman LH. Cell Wall Deficient Forms: Stealth Pathogens, 3rd edn. Boca Raton, FL: CRC Press, 2001).

Bystander or perpetrator?

Nevertheless, although L-forms are invariably present at the scene in a multitude of chronic diseases, it does not necessarily mean that they are the cause of the condition. However, the fact that the L-form is a pathogen suggests, by definition, that it does cause disease, and this was demonstrated as early as in the 1920s by pathologist John Nuzum, at the University of Illinois College of Medicine.

Nuzum isolated bacteria of a genus that he called 'Micrococcus' from breast-cancer tumours and, in a series of dangerous experiments, he injected these microorganisms into the leg of a 70-year-old man who, after 62 such injections, began to develop skin cancer (Surg Gynecol Obstet, 1921; 33: 167-75). Thirty years after Nuzum carried out his experiments, Irene Diller, at the Institute for Cancer Research at Fox Chase in Philadelphia, PA, independently discovered fungus-like microbes in cancer cells. She injected these cells into laboratory mice and found that the injected mice had twice the number of cancers as mice that were not injected (Growth, 1962; 26: 181-209).

More recently, Dr Andy Wright, from the Complete Hormone Clinic in Bolton, UK, discovered that L-forms are responsible for chronic fatigue syndrome (CFS). Using a special microscope, and special immune stains when necessary, Wright has been able to isolate and visualize L-forms in every one of the 600 cases of CFS that he has examined. He has even filmed the isolated L-forms changing shape as they weave in and out between cells and has shown that, when they become rectangular, they enter the cell and begin to grow.

His findings have been confirmed by Danish researcher Marie Kroun (see Bacteriality: Exploring Chronic Disease, at http://bacteriality.com/ 2007/08/18/history). As a result of these findings, Wright postulates that CFS/myalgic encephalomyelitis (ME) are bacterial diseases caused by L-forms.

What's more, a team of scientists led by Australian biomedical researcher Trevor Marshall has also independently confirmed Wright's discovery, and has demonstrated how L-form bacteria are able to destabilize the healthy functioning of the immune system and persist in the body (Autoimmun Rev, 2009; 8: 677-81; doi: 10.1016/j.autrev.2009.02.016).

Toxic thinking

For the past century, every scientist who postulated the cancer-bug theory has been ignored, vilified, had their funding stopped or, in the case of Wilhelm Reich-who developed his own peculiar take on bacteria and cancer-been imprisoned.

In her autobiography, Florence Seibert wrote: "It is very difficult to understand the lack of interest, instead of great enthusiasm, that should follow such results . . . The contrast between the progress made in tuberculosis, where we know the cause, where we have good general diagnostic tests, where we have a vaccine and effective antibiotic controls, and that made in cancer with the millions invested, is very striking. Some dedicated scientists should indeed find it rewarding to confirm or deny these painstaking and time-consuming experiments, for the sake of establishing the first necessary step in the important problem of the etiology of cancer" (Seibert F. Pebbles On the Hill of a Scientist. St Petersburg, FL: privately published, 1968).

Although the cancer-bug theory continues to be generally ignored, medicine has few answers of its own against cancer. The cancer rate continues to increase, so that it now afflicts more than one in three people, and the therapies that are available appear to work poorly or hardly at all.

Instead of focusing on the tumour-which is merely the mani-festation, or symptom, of a process-the cancer-bug theory calls for a new therapy that seeks to reverse the development of the process that starts with infection, and then progresses
to inflammation and, eventually, cell alteration. Restoring cellular balance would be the clarion call of the new cancer therapy.
Eminent scientists over the last one hundred years have repeatedly demonstrated the very real possibility that a pleomorphic bug is involved in cancer, but any impartial observer is likely to conclude that money, reputation or dogma-or a toxic mix of the three-clearly matter more than an open-minded approach to solving one of mankind's greatest scourges.

Bryan Hubbard

WDDTY VOL 21 NO 3


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