E. coli gut infection linked to bowel cancer

A common type of gut bacterium may increase a person's chance of developing bowel cancer, according to a study published in the journal Nature.

By Michelle RobertsHealth editor, BBC News online

• 27 February 2020

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A common type of gut bacterium may increase a person's chance of developing bowel cancer, according to a study published in the journal Nature.

The bacterium is a type of E. coli infection, present in up to one in five people, scientists believe.

It releases a toxin which experts say can damage the cells that line the bowel, potentially turning some cells cancerous over time.

There are around 42,000 new cases of bowel cancer each year in the UK.

Experts do not yet know how many of these might be linked to the E. coli strain that makes the toxin colibactin.

• Bowel cancer rates rising 'among young adults'
• Dame Julie Walters reveals shock of bowel cancer diagnosis

How dangerous might it be?

The researchers suspect it may contribute to a minority of bowel cancer cases - one in 20 or five in every 100 - but more research is needed to confirm the link.

There is no routine test for the bacterium currently, and it is not clear yet that people who have it will be at heightened risk.

In some people it may live in the bowel and cause no issue.

It is not the first infection to be linked with cancer, however. HPV is a virus that causes cervical cancer and H pylori infection is associated with stomach cancer.

Is it the same as food poisoning?

No. This particular E. coli strain is not one of the ones linked to food poisoning outbreaks.

There are lots of different types of E. coli. Many are part of the normal gut flora - the trillions of bacteria that naturally live in the bowel.

What did the study find?

The team, from The Netherlands, the UK and the US, used miniature replicas of the human gut, grown in the lab, to test the effects of the toxin on cells.

They then compared the damage seen with more than 5,000 bowel cancer samples taken from patients and found identical patterns or "fingerprints" of DNA damage in around 5% of the samples.

What are bowel cancer symptoms?

• a persistent change in bowel habit - going more often, with looser stools and sometimes tummy pain
• blood in the stools without other symptoms, such as piles
• abdominal pain, discomfort or bloating always brought on by eating - sometimes resulting in a reduction in the amount of food eaten and weight loss

Most people with these symptoms do not have bowel cancer, but the NHS advice is to see your GP if you have one or more of the symptoms and they have persisted for more than four weeks.

Source: NHS UK

How do the findings help us?

Experts say it may be possible to develop a more sensitive test to detect early bowel tumours using this knowledge about the toxin.

The findings may also offer a way to prevent some bowel cancers, by getting rid of the bacterium from the body before it can do any harm, using existing antibiotics.

One of the researchers, Prof Hans Clevers, from the Hubrecht Institute in The Netherlands, said: "Common antibiotics will kill these bacteria.

"This is the first time we've seen such a distinctive pattern of DNA damage in bowel cancer, which has been caused by a bacterium that lives in our gut."

He said there may be other gut bacteria that do the same.

Probiotic treatments that contain a similar strain of E. coli, called Nissle 1917, might also pose a risk potentially, he added - but these are not the same ones found in yoghurt drinks sold in supermarkets.

"Although it might sound scary, there's still lots left to understand about our how our gut bacteria affect our health, what we could do about it, and how much impact it has on bowel cancer risk," says Nicola Smith, senior health information Manager at Cancer Research UK, who funded the work.

"In the future, knowing what role bacteria in our gut plays could change the way we detect and prevent bowel cancer.

"But we do know that around half of bowel cancer cases can be prevented by not smoking, keeping a healthy weight and eating a balanced diet - so there's plenty of changes that you can make right now that will reduce your risk," she added.

Genevieve Edwards, chief executive at Bowel Cancer UK, said: "Although this research is at an early stage, it adds to the growing body of evidence about the role that bacteria and other microorganisms that live in our gut may play in bowel cancer development. "

https://www.bbc.com/news/health-51626946

Exclusive Report from the American Association for Cancer Research Conference

Most cancers are preventable with lifestyle alterations. Scientists at the annual meeting of the American Association for Cancer Research report on a variety of research topics relating to reducing cancer risk and improving oncology treatments.

September 2016

By Ben Best

Most forms of cancer are almost entirely preventable. No more than 10% of cancer cases can be attributed to inherited genetic factors, while 90%-95% are caused by lifestyle and environmental factors.1

Tobacco alone accounts for 25%-30% of cancer deaths, diet for 30%-35%, infections for 15%-20%, and radiation (including ultraviolet light) up to 10%.1 Being overweight or obese is estimated to cause 4%-20% of cancer deaths.2 All of these factors create or lead to chronic inflammation,3 the most common cause of cancer.1,4

Cells in body tissues are normally “good citizens” that cooperate with other cells to facilitate body function. Cancer cells, by contrast, have no purpose other than to grow and multiply, contributing nothing to body function.

Many cancers are based on abnormal DNA or chromosomes, usually due to lifestyle or environmental DNA damage, but some are the result of inherited mutations.5 For example, although mutations in the BRCA1 gene are not common for the general population,6,7 for those having it, the risk of breast or ovarian cancer before the age of 70 is 65% or 39%, respectively.8 (It’s possible that lifestyle differences have some bearing on which BRCA1 carriers do or do not get cancer, but this has not been well studied.)

The two broad classes of genetic defects underlying cancer are (1) overactive oncogenes (genes that accelerate growth and multiplication), and (2) inactivated tumor suppressor genes (genes that normally prevent cancer).

Two of the most common oncogenes are PIK3CA (which promotes cell growth, survival, and motility)9 andKRAS (which greatly increases cell glucose uptake).10 The most common tumor suppressor gene is p53(which causes cells with defective DNA to self-destruct or stop replicating).11

Cancer begins with gene mutations that increase abnormal growth and replication. Factors that assist these processes enable cancer cells to immortalize, or promote the formation of new blood vessels to nourish the tumor. In more advanced stages, mutations allow cancer to spread to other organs, a process called metastasis. More than 90% of cancer deaths are due to metastasis.12 To reach the metastatic stage typically requires at least several mutations.13 The risk of cancer before age 40 is only about 2%, but by age 80 the risk increases to 50%.14

In the United States, the six most frequently diagnosed cancers are, in decreasing order: breast, lung, prostate, colorectal, bladder, and skin. The six most common causes of cancer death in the United States are, in decreasing order: lung, colorectal, pancreas, breast, prostate, and liver.15 Thanks to aggressive efforts to detect breast and prostate cancer in early stages, they are often cured. Pancreatic cancer, by contrast, is usually only detected in more advanced stages.

Normal cells generate most of their energy from glucose and oxygen in the mitochondria. Cancer cells, however, obtain their energy by glucose metabolism outside the mitochondria through glycolysis. Although it is 18 times more efficient to derive energy from glucose in mitochondria,16 cancer cells compensate by absorbing massive amounts of glucose, with rates of glycolysis up to 200 times greater than normal cells.17

Cancer cells use glucose primarily as a source of material for building cellular components, rather than for energy.17,18 High glucose utilization is so characteristic of cancer that cancer imaging with PET scans is based on detection of high glucose utilization.19

Dichloroacetate (DCA), a non-patented compound, counteracts a protective mechanism used by cancer cells that prevents glucose products from entering mitochondria, which would send the mitochondria into overdrive, resulting in cell death.18 Life Extension Foundation® is funding clinical trials to treat cancer patients with DCA.

With this background, let’s review the American Association for Cancer Research annual meeting, which was held April 18-22, 2015, in Philadelphia.

Colorectal Cancer

Grivennikov

Sergei Grivennikov, PhD, assistant professor, Fox Chase Cancer Center, Philadelphia, is a specialist in cancers of the large intestine and rectum. He provided insights on the most frequently mutated gene in colorectal cancer, the adenomatous polyposis coli (APC) gene. This defect is seen in 75% of sporadic colorectal cancers, but is due to an inherited mutation in less than 1% of cases.20

Chronic inflammation, characterized by the release of inflammatory cytokines (proteins) and DNA-damaging oxidants is typically the cause of colorectal gene mutations. Chronic inflammation not only contributes to the initiation of cancer mutations, but to tumor growth and metastasis.12 Inflammation leads to infiltration of bacteria into tumors, which enhances the inflammation by releasing endotoxins.21-23 A high-fat diet can result in excessive pro-inflammatory bile acids, which can increase cancer-causing bacteria.24 Calcium can help remove toxic bile acids.25,26

Trinchieri

Giorgio Trinchieri, MD, director for the Cancer and Inflammation Program, National Cancer Institute, Bethesda, Maryland, is concerned with the fact that inflammation contributes to abnormal bacteria in the gut, and that the abnormal bacteria interfere with anticancer chemotherapy.27 Dr. Trinchieri would like to alter the gut microbiota to improve cancer treatment.28 He recommends the use of probiotics, prebiotics, and transplantation of feces from healthy persons into cancer patients.29 The FDA has been blocking fecal transfer by insisting that human stools are a drug which will require FDA approval before it can be given to patients.30

Jobin

Christian Jobin, PhD, professor of medicine, University of Florida, Gainesville, is concerned with how inflammation induces colorectal cancer. Death from colorectal cancer is at least twice as high in persons with ulcerative colitis or Crohn’s Disease as for the general population.31 Dr. Jobin suggests that inflammation encourages expansion of gut microorganisms that can induce cancer,32 including more toxic strains of E. coli bacteria.33 Even without increasing the number of E. coli, inflammation can increase the propensity of E. coli to induce colorectal cancer.34 Dr. Jobin wants to develop bacteria-killing viruses that are specific for the toxic strains of E. coli most responsible for inflammation and cancer.

Aspirin against Colorectal Cancer

Andrew Chan, MD, program director, Gastroenterology, Massachusetts General Hospital, Boston, has investigated the use of aspirin to prevent colorectal cancer and to improve survival in colorectal cancer patients. Dr. Chan found that women who took the largest amounts of aspirin (325 mg more than 14 times per week) had the greatest (53%) reduction in risk of colorectal cancer.35 But he also found that those women had the highest risk of gastrointestinal bleeding.36 Dr. Chan discovered that aspirin increased survival in colorectal cancer patients with a PIK3CA mutation, but not in patients lacking this mutation.37 Dr. Chan has done genetic screening to better identify colorectal cancer patients who would or would not benefit from aspirin.38 Editor’s note: Studies using lower dose aspirin reduce cancer risk, but not as effectively (by 53%) as reported by Dr. Chan.98,99

Cervical Cancer

Douglas Lowy, MD, acting director, National Cancer Institute, Bethesda, Maryland, works on vaccination against human papillomavirus (HPV). HPV is nearly always the cause of cervical cancer,39 which is the second most common cause of cancer in women worldwide.40 HPV is almost twice as common in less developed countries compared to developed countries,41 and is the most common sexually transmitted infection, although symptoms are not usually manifest.42 A school HPV vaccination program for girls aged 12-17 was introduced in Australia in 2007. Prevalence of the types of HPV vaccinated against dropped to less than a quarter of the initial value in young women by 2011,43 and genital warts among women under 21 dropped from over 11% to less than 1%.44 DNA testing for HPV provides 60%- 70% better screening than Pap smears.45

The PIK3CA Oncogene Mutation

Vanhaesebroeck

Bart Vanhaesebroeck, PhD, professor, University College London Cancer Institute, London, England, is interested in the PIK3CA subset of PI3K ( PhosphoInositide 3-kinase) as one of the most frequently mutated genes in cancer, occurring in up to 40% of breast cancer cases, more than a third of cancers of the uterus, up to a third of colon cancers, and about a quarter of stomach cancers (among other cancers).46These mutations in PIK3CA result in excessive cell growth, multiplication, metastasis, and inhibition of apoptosis (cell suicide).9 PIK3CA mutations are one of the most common oncogene mutations in breast cancer (especially cases associated with increased estrogen response).47 PIK3CA-inhibiting substances can not only reduce PIK3CA activity,48 but normalize blood vessels, thereby facilitating delivery of other chemotherapeutic agents.49

Cancer Stem Cells

Kolev

Vihren Kolev, PhD, senior scientist, Verastem, Inc., Cambridge, Massachusetts, is attempting to eliminate cancer by targeting cancer stem cells. These cells are hard to eliminate. Often, apparently successful eradication of tumors by chemotherapy ultimately ends in failure because surviving cancer stem cells create a new, more resistant tumor. He described markers of cancer stem cells, such as focal adhesion kinase50 and aldehyde dehydrogenase 1,51,52 which have the possibility of making stem cells easier to locate and identify, and thus eliminate.

SIRT6 Protects Against Cancer

Mostoslavsky

Raul Mostoslavsky, MD, PhD, associate professor of Medicine, Harvard Medical School, is an expert in sirtuin proteins,53 the most well-known of which is SIRT1. SIRT1 extends the lifespan of yeast, worms, and flies when stimulated by resveratrol.54 Dr. Mostoslavsky, however, is most interested in the effect of SIRT6 on cancer. SIRT6 is localized at the telomeres at the end of chromosomes. It helps to maintain genetic stability, and prevents cellular aging.55 Dr. Mostoslavsky has demonstrated that SIRT6 maintains genetic stability by assisting with repair of damaged DNA.56 Cancer cells are greatly dependent on glycolysis to support rapid growth and multiplication. Dr. Mostoslavsky has shown that SIRT6 opposes this process, that reduction of SIRT6 fosters glycolysis, and that many cancers repress SIRT6.57 Life Extension Foundation is funding Dr. Vera Gorbunova to find SIRT6-activating therapies.

Enhancing the Immune System against Cancer

Schumacher

Ton Schumacher, PhD, professor, Netherlands Cancer Institute, Amsterdam, Netherlands, works on using the immune system to fight cancer. The role of the immune system in preventing cancer is apparent from the fact that AIDS victims and transplant recipients taking immune suppressant drugs have an increased risk of cancer.58,59 Cancer cells are able to evade or suppress the immune system. The journal Science called cancer immunotherapy the “breakthrough of the year” in 2013 because of the discovery of ways to prevent cancer from blocking the immune system.60 Cancer that has spread from its tissue of origin (metastatic cancer) is generally incurable. Metastatic melanoma has shown rapid tumor regression in nearly a third of patients receiving these kinds of immunotherapies (checkpoint inhibitors) that prevent cancer from blocking the immune system.60 Dr. Schumacher was part of a team that analyzed nearly five million mutations in over 7,000 cancers. Melanoma and lung cancer were found to have the highest frequency of mutations.61 Cancer cells that have the highest number of mutations, such as melanoma, are the most vulnerable to this type of (checkpoint inhibitor) immunotherapy.62

CRISPR Gene Editing to Fight Cancer

 

Tyler Jacks, PhD, director, Koch Institute for Integrative Cancer Research, Cambridge, Massachusetts, has been using the new CRISPR/Cas9 technology, which was developed for editing the human genome in 2013.63,64 CRISPR/Cas9 is based on a system used by bacteria to defend themselves against viruses. When bacteria are invaded by viruses, the bacteria store part of the virus’s DNA in the genome of their cell, called CRISPR. RNA copied from the CRISPR is attached to a Cas9 cutting enzyme. The RNA then guides the Cas9 enzyme to the virus to cut (and thereby destroy) the virus. CRISPR/Cas9 has been applied to gene editing by designing guide RNAs for specific DNA locations to be edited.63

Dr. Jacks has worked on a team that used CRISPR/Cas9 to cure an inherited disease in a mouse.65 He has also used CRISPR/Cas9 to create a mouse model of cancer.66 Such models can be used to study the features of many cancer types, and to experiment with potential therapies. Cancer cells can have a high mutation rate, although only a few of the mutations are thought to drive the cancer. CRISPR/Cas9 can be used to distinguish between mutations that drive cancer and mutations which do not. Dr. Jacks anticipates that CRISPR/Cas9 will be used to design immune system cells that target specific cancers.67

Conclusions/Interpretations

 

It is an unfortunate fact that almost all of modern medicine is based on treatment of disease, rather than on prevention, most tragically exemplified by cancer, which is so highly preventable. The key to prevention is better lifestyle. Unconventional health practices have the potential to reduce cancer incidence even more than the lifestyle changes advocated by conventional medicine. As I wrote in the December 2015 issue of Life Extension Magazine®, a low carbohydrate ketogenic diet can provide energy while depriving cancer cells of the amount of glucose they require.

Conventional medicine too often discounts the value of supplements, but many scientific studies demonstrate that supplements can substantially reduce cancer incidence.1

The key to more curative treatment is early detection. Good breast and prostate examination practices explain why the diagnosis rate for these cancers greatly exceeds the rate of fatality. Colon cancer would be more effectively treated if more people had regular colon examinations. Liver cancer is often due to chronic inflammation resulting from hepatitis. The hepatitis B virus can be prevented by vaccination.68 Hepatitis C virus is usually transmitted by unsafe intravenous drug or transfusion practices and unprotected sex, but is now controlled in over 90% of cases.69,70 Pancreatic cancer has been difficult to detect in early stages, which is why it is so often fatal. Cancer cells often release DNA into the bloodstream, which means that detecting cancer through blood tests (“liquid biopsies”) may be done in the future if standardized techniques can be developed.71

Notes on Cancer Prevention

There appears to be a link between salt intake and the bacterium Helicobacter pylori, which is associated with stomach cancer. It is possible that these two factors contribute to the development of the disease. In addition, salt intake and other dietary components are likely to damage the stomach mucosal lining, increasing the risk of stomach cancer.72 Risk of stomach cancer, colon cancer, and rectal cancer is probably increased by damage to mucous membranes from iron or N-nitroso compounds (NOCs) in red or processed meat.73-75Further damage is caused when cooking at high temperatures as this contributes to the formation of cancer-causing heterocyclic amines.76 Mucosal damage is also a reason why consuming more than two drinks of alcohol daily increases colorectal cancer risk.77 Any amount of alcohol consumption increases the risk of breast cancer in women because alcohol can convert estrogen into carcinogenic forms.78-81 For women with a BRCA1 mutation, surgical removal of the breasts can result in a reduced breast cancer risk.82,83

Animals that eat plants and fish that eat fish have increased concentrations of toxic metals in their flesh84,85and increased concentrations of organic toxins in their fat.86-88 Organic toxins like PCBs (polychlorinated biphenyls) persist in the environment and thus accumulate in fat tissue, increasing by many times the risk of melanoma skin cancer (for example).89 Because these toxins can damage DNA and cause cancer, a plant-based diet is safer than an animal-based diet. Chlorophyllin supplements can reduce the cancer-causing potential of toxin exposure.90,91 (See the December 2015 issue of Life Extension Magazine for more details.)

Selenium supplementation has been shown to reduce cancer incidence.92 A double-blind, randomized study showed that zinc supplements improved survival of cancer patients receiving radiation therapy.93 Vitamin D supplementation has been shown to reduce breast cancer incidence.94 Curcumin has been shown to inhibit breast cancer metastasis in mice.95 Higher quercetin intake is associated with reduced lung cancer incidence.96 A randomized, placebo-controlled trial of omega-3 fatty acid (EPA) supplementation showed significantly reduced polyp formation in subjects having an inherited predisposition to colon cancer.97 Life Extension Magazine has published many articles about nutrients which can reduce DNA damage by preventing inflammation and adverse gene expression changes, so the above is merely a sampling.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.

http://www.lifeextension.com/Magazine/2016/9/Exclusive-Report-from-the-American-Association-for-Cancer-Research-Conference/Page-01

How Curcumin Protects Against Cancer - Life Extension

As mainstream oncology misguidedly focuses on toxic, single-agent treatments, a wealth of compelling data puts curcumin at the forefront of multimodal cancer prevention.

Life Extension Magazine®
Issue: Mar 2011

According to the American Cancer Society,1 one out of every three women in the United States risks developing some form of cancer over the course of their lives. For men, that number rises to one in two. Since cancer is an age-related disease, the risk of diagnosis increases the longer one lives, making it the second leading cause of death in this country.2,3

These data underscore a stark reality. When it comes to cancer prevention, the medical establishment and drug company profiteers remain grossly negligent in protecting the public. The result is countless avoidable cancer deaths each year. There is an urgent need to provide aging individuals with validated interventions to target cancer’s multiple causative factors before they take hold.

Among the most compelling and underrecognized of these is curcumin. In contrast to mainstream oncology’s focus on single-agent toxic treatments, curcumin has emerged as a potent multimodal cancer-preventing agent, with 240 published studies appearing in the global scientific literature in the past year alone.

In this article, you will learn of the multiple factors involved in carcinogenesis (cancer development). You will discover up-to-date research demonstrating curcumin’s power to disrupt specific molecular mechanisms that lead to cancer—and to even treat the disease in many cases.

System-Wide, Safe, Multimodal Defense

Curcumin is derived from the Indian spice turmeric and possesses several active components, all of which contribute to its anti-inflammatory and chemopreventive power.4-6 In fact, curcumin targets ten causative factors involved in cancer development.

Disrupting any one of these factors gives you a good chance of preventing cancer; disrupting several provides even greater protection, including the prevention of DNA damage.7

By blocking the inflammatory master molecule nuclear factor-kappaB (or NF-kB), curcumin blunts cancer-causing inflammation, slashing levels of inflammatory cytokines throughout the body.8,9 Curcumin also interferes with production of dangerous advanced glycation end products that trigger inflammation which can lead to cancerous mutation.10

Curcumin alters cellular signaling to enhance healthy control over cellular replication, which tightly regulates the cellular reproductive cycle, helping to stop uncontrolled proliferation of new tissue in tumors.11 It promotes apoptosis in rapidly reproducing cancer cells without affecting healthy tissue11-13 and reins in tumor growth by making tumors more vulnerable to pharmacologic cell-killing treatments.11,14

In addition, curcumin regulates tumor suppressor pathways and triggers mitochondrial-mediated death in tumor tissue, thereby increasing the death of cancer cells.11,15

Finally, curcumin interferes with tumor invasiveness and blocks molecules that would otherwise open pathways to penetration of tissue.2 It also helps to starve tumors of their vital blood supply and it can oppose many of the processes that permit metastases to spread.8,16,17 These multi-targeted actions are central to curcumin’s capacity to block multiple forms of cancer before they manifest.

Combating Deadly Cancers in Women

Breast cancers vary widely in their responsiveness to standard treatment. Cancers that depend on the hormone estrogen for survival are more effectively treated with conventional methods. Those that lack receptors for female hormones are far more resistant to treatment. This is where curcumin’s value truly lies, because it has the ability to induce apoptosis (programmed cell death) in a variety of hormone-negative cancers.18-20 Remarkably, curcumin produces virtually no change in healthy breast cells, with very low toxicity even at doses as high as 8,000 mg daily.21

In human cancer patients, curcumin doses as high as 3,600 mg a day have been shown to induce the following favorable anti-cancer effects:

• Paraptosis. A process similar to apoptosis (programmed cell death), curcumin initiates paraptosis only in breast cancer cells, resulting in their rapid destruction.22
• Targeted destruction of cancer-cell mitochondria (leaving mitochondria in healthy cells unaffected).22
• Disruption of the cancer cell cycle. Curcumin can “suspend” cancerous cells in a non-reproductive state within their life cycle, thereby halting their replication.20,23-25
• Cancer cell downregulation. Curcumin blocks a group of molecules vital to the process of metastasis. In animal models, it has been shown to reduce metastatic spread to the lungs via this pathway.17,26,27
• Arrested stem cell development. Curcumin inhibits growth and renewal of so-called cancer stem cells, aberrant cells now believed to be at the root of many cancers, including breast cancer.3,28

Curcumin has also been shown to effectively combat cervical cancer, a leading cause of cancer death in women in developing nations and a common cancer in this country.29 It is caused largely by infection with the human papilloma virus, or HPV. Curcumin’s anti-inflammatory effects break the link that triggers HPV-induced cancer development.29,30

Curcumin further promotes apoptosis of cancer cells within the lining of the uterus and reduces the growth rate of painful but non-malignant uterine leiomyomas (uterine fibroids). 31-34

Collectively, these effects make curcumin attractive both as a primary chemopreventive agent in women at risk for breast cancer and an adjuvant treatment option in those who have already developed the disease.20,21

Prostate Cancer Defense

Prostate cancer is the second leading cause of cancer death in American men.35,44 Fortunately, its long latency period and slow growth rate make it a prime candidate for prevention.36 Curcumin strikes at multiple targets in prostate malignancies, interfering with the spread of cancer cells and regulating inflammatory responses through the master regulator NF-kB.36-38

Like certain breast cancers, prostate cancer is often dependent on sex hormones for its growth. Curcumin reduces expression of sex hormone receptors in the prostate, which speeds androgenic breakdown and impairs cancer cells’ ability to respond to the effects of testosterone.39-42 It also inhibits cancer initiation and promotion43 by blocking metastases from forming in the prostate and regulating enzymes required for tissue invasiveness.44

Combating Gastrointestinal Cancers

Colorectal cancer is the third most common malignancy in adults and the second leading cause of cancer deaths.45,46 Despite aggressive surgical care and chemotherapy, nearly 50% of people with colorectal cancers develop recurrent tumors.47 This may be due in part to the survival of dangerous colon cancer stem cells that resist conventional chemotherapy and act as “seeds” for subsequent cancers.3,48,49

On the other hand, these cancers are excellent candidates for prevention, since they follow a predictable sequence from non-malignant polyps to full-blown cancerous growths, usually requiring a decade to develop.46

Much as with malignancies of the breast, cervix, and prostate, curcumin slows the progression from colon polyp to cancer by damping down the inflammatory cascade triggered by NF-kB and pro-inflammatory cytokines.6 This halts the growth of cancer cells before they can become detectable tumors via a host of interrelated molecular mechanisms.50,51

Curcumin also creates a gastrointestinal environment more favorable to optimal colon health by reducing levels of so-called secondary bile acids, natural secretions that contribute to colon cancer risk.52 That has a direct effect, inhibiting proliferation of cancer cells and further reducing their production.53

Curcumin also suppresses colon cancer when combined with other polyphenols such as resveratrol.46,54 The combination of curcumin with green tea extracts has prevented experimentally induced colon cancer in rats.55

Curcumin also synergizes with standard chemotherapy drugs, helping to boost their efficacy and potentially reduce the dose of toxic chemotherapy products, minimizing needless harm and suffering for cancer patients.45,47-49 Curcumin increases colon cancer cell response to radiation.56

A novel feature of curcumin is its ability to bind to and activate vitamin D receptors in colon cells.57 Vitamin D is known to exert potent anti-cancer properties.

Curcumin is equally powerful at preventing cancers in the stomach. It inhibits growth and proliferation of human gastric cancer cells in the laboratory and is particularly effective in stopping cancers that have become resistant to multiple drug treatment.58-60 Curcumin can prevent gastric cancer cells from progressing through their growth cycle, blocking further tumor growth.60

Infection with the bacterium Helicobacter pylori (H. pylori) is a known cause of gastritis, peptic ulcer, and gastric cancer.61 Curcumin blocks growth of H. pylori and reduces the rate at which stomach cells react by turning cancerous.61,62 This effect is again related to curcumin’s fundamental ability to block activation of inflammatory NF-kB.62

WHAT YOU NEED TO KNOW: MULTIMODAL ANTI-CANCER POWER OF CURCUMIN

Curcumin has emerged as a potent cancer-preventing agent, with 240 published studies appearing in the global scientific literature in the past year alone. Its multimodal effects act to simultaneously counter ten discrete causative factors in cancer development. It intervenes at each stage in the complex sequence of events that enable cancer cells to develop, proliferate, and metastasize. Its multitargeted mechanisms of action have yielded compelling results in combating a remarkably broad array of cancers, including those of the breast, uterus, cervix, prostate, and GI tract. A blossoming body of research reveals curcumin’s promise in countering cancers of the blood, brain, lung, and bladder as well.

Further Preventive Potential

Curcumin’s anti-inflammatory, antioxidant, and gene-regulating powers have been explored in preventing or treating cancers of the blood-forming system (leukemias, lymphomas, and myelomas) as well as those of the brain, lung, and bladder.12,13,63-81 Even aggressive tumors of the head and neck, often following years of smoking, are proving responsive to curcumin treatment.14,82-85 Curcumin is also emerging as a potentially effective intervention for pancreatic cancer—one of cancer’s most lethal and aggressive forms.86-90

Summary

Cancer is the second leading cause of death in the US, and the risk of developing the disease increases significantly as we age.

Curcumin has emerged as a potent cancer-preventing agent, with 240 published studies appearing in the global scientific literature in the past year. Curcumin’s multimodal effects act to simultaneously counter ten discrete causative factors in cancer development.

It intervenes at each stage in the complex sequence of events that must occur in order for a cancer to develop, progress, invade, and ultimately metastasize to healthy tissue.

The multi-targeted mechanisms of curcumin have yielded compelling results in combating a remarkably broad array of cancers, including those of the breast, uterus, cervix, prostate, and GI tract. A burgeoning body of research demonstrates curcumin’s potential to counter cancers of the blood, brain, lung, and bladder as well.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at
1-866-864-3027.

Ten Key Causative Factors in Cancer Development More than many other age-related diseases, cancer results from the cumulative effect of years of discrete, small-scale assaults on the body. Oxidation, inflammation, stress, infection, and other physiological insults take their toll, inflicting lethal damage over time that sets abnormal cell proliferation in motion.91,92 1. DNA damage. Numerous biomolecular assaults strike at the “blueprint” that cells need in order to replicate themselves accurately. DNA damage is often referred to as the “initiator” in cancer development—the first step in the onset of most cancers. 2. Excessive or chronic inflammation. Inflammatory processes trigger the release of a host of disruptive cytokines (cell-signaling molecules) that affect virtually all cellular functions. Inflammation is commonly referred to as a cancer “promoter” for this reason. 3. Disruption of cell signaling pathways. Normal communication within and between cells assures proper regulation of their healthy function. These pathways are easily disrupted by adverse events such as inflammation. 4. Alterations in the cellular reproductive cycle. Cells undergo a four-stage process as they prepare to replicate themselves. The cell cycle itself is controlled by signaling pathways that can be altered or disrupted at each of these stages. 5. Abnormal regulation of apoptosis. Apoptosis is the process of naturally “pre-programmed” cell death that prevents overgrowth of tissue. When apoptosis fails, cells may undergo uncontrolled reproduction. 6. Altered survival pathways. The flip side of unregulated apoptosis: survival of too many healthy cells, paradoxically, can endanger the host by permitting a cancer to take hold by increasing the odds of mutation and proliferation. 7. Excessive cellular proliferation. Certain hormones and other stimuli can directly trigger cells to reproduce without safe limits, especially when the preceding regulatory mechanisms have failed. 8. Aggressive invasion of healthy tissue. This is accomplished by excessive production of enzymes and adhesion molecules that “dissolve” tissue and allow the tumor to literally take root. The word “cancer” itself is derived from the crab-like appearance of fully-developed malignancies, which extend tendrils in all directions into healthy tissue.93 9. Rapid angiogenesis. Tumors require growth of new blood vessels for nourishment. They are endowed with the capacity to spontaneously generate new blood vessels just like healthy tissue. Angiogenesis in cancer tissue is a primary means by which tumors grow. 10. Metastasis. This is the migration of cancerous cells to regions of the body beyond the locus of the primary tumor. Metastases are the distinguishing features of most malignant cancers, and the typically herald the onset of end-stage disease because they disrupt otherwise healthy tissues.

References

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