IHMT for Cancer Treatment and Prevention

Mitchell L. Gaynor, MD

Cancer Syllabus

What is Integrative Oncology?

Integrative oncology is the combination of conventional and complementary interventions into an individualized therapeutic regimen that addresses the whole person (mind/body, spirit, and community) living with and beyond cancer (Clinical Advances in Hematology & Oncology. 2007;5:45-47).

Goals and Methods of Integrative Oncology

• Nutritional modulation of factors specific to cancer
• Vitamin/supplement/juicing/superfoods
• Ameliorate nausea and appetite problems
• Provide optimal nutrition during cancer treatment
• Reduce fatigue and improve energy
• Metabolic, heavy metal, and endocrine profiles
• Nutrients to decrease inflammation
• Guidelines during radiation and chemotherapy
• Stress reduction

Philosophy of Gaynor Integrative Oncology

We must feed the parts of our bodies capable of fighting cancer, and at the same time starve the body of those ingredients that leave it most receptive to cancer. The main things to reduce or eliminate are refined sugar and saturated fat.

Cancer—Promoters and Deterrents

Obesity and Dietary Associations

The majority of malignancies are associated with obesity. A 2003 study (New England Journal of Medicine. 2003;348 p.1625-138) investigated more than 900,000 subjects over the age of 16. The investigators reported that obesity was indeed related to mortality for the common cancers (including breast, prostate, colon, and pancreas), because it caused high circulating insulin levels. The ACS Cancer Prevention Study (Am J Epidemiol. 2004;159(12):1160-1167) followed more than 400,000 women for 14 years, demonstrating that obesity results in a 40 to 50% increased risk of breast cancer.

Sugar has been found to markedly depress the immune system, specifically the very parts involved in killing cancer cells before they become clinically apparent. The functional ability of the T cell, for example, drops by about half after a high sugar intake and stays depressed for hours. A high sugar diet is also linked to obesity and adult-onset diabetes. Both of these conditions have been linked to a higher risk of breast and colon cancer. Furthermore, sugar intake (especially the simple, refined sugars found in candy and white sugar) causes your body to respond by making more insulin. Many cancer cells have insulin receptors on their surfaces, resulting in cancer cell growth in response to higher insulin levels. Insulin also controls the proteins which bind to estrogen circulating in the blood. The higher the insulin, the fewer the proteins which bind estrogen. Thus, higher insulin means more free estrogen. As we will discuss, both these initiate cell division in breast and other cancers. Alcohol has a high glycemic index, meaning a lot of insulin must be secreted for its metabolism. More than two drinks per day increases a woman’s risk of breast cancer by over 50%.
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An interesting laboratory study by Massachusetts researchers (J Agric and Food Chemistry. 2007;55(1):99-105) showed that the enzyme alpha glucosidase, which is responsible for supporting the absorption of sugar in the gut, is dramatically inhibited by black tea. This may well have implications not only for diabetes, but breast cancer prevention as well. Black tea extracts had the greatest inhibitory effect on alpha-glucosidase, followed by white tea and oolong tea. Since many new diabetes drugs such as acarbose are aimed at inhibiting this enzyme super sugar absorber, a tea bag may be the next sugar-busting nutrient!

Does a diet rich in refined sugar and meat really increase your risk of breast cancer? Most studies show a decreased survival in patients with breast cancer who eat a high saturated fat diet. A study in the Journal of the Cancer Institute showed that when women were put on a low-fat diet, their levels of estradiol dropped 17% over a 2-year period (JNCI. 1990;82(2):129-134). This would mean an even greater decline in breast cancer risk since estradiol levels correlate with breast cancer risk. A 2003 Journal of Nutritional Cancer Institute study of over 90,000 women showed premenopausal women consuming the highest saturated fat diets have an elevated breast cancer risk compared to women eating the lowest amount of these fats (JNCI. 2003;95(14):1079-1085).

The multicenter Shanghai Breast Cancer Study, published in 2007 (Can Epidem Biomarkers Prev. 2007;16:1443), provided a look at a population of Chinese women who were beginning to adopt Western-style dietary habits. The subjects were divided into two groups: the “meat-sweet” group (primarily eaters of pork, beef, poultry, candies, and desserts), and the “soy-vegetable” group (those who primarily ate various vegetables, soy products, and freshwater fish). Those in the “meat-sweet” group who were overweight had more than double the estrogen receptor positive breast cancer risk as those in the “soy-vegetable” group. The study reinforces the need for women to be within 10% of their ideal body weight and limit intake of meats and refined sugars.

Studies show diets high in saturated (animal) fats (red meat and dairy) increase a woman’s risk of breast cancer by 50% (NEJM. 1987;316(1):22-28). A study published in Annals of Oncology (2001;12(11):1533-1538) reviewed dietary habits of more than 5,000 women, finding a direct association between glycemic load and breast cancer risk. When patients say, “Well, doc, since everything is bad for me, I just can’t worry,” I say, “Try then at least to avoid the worst.” Sugar is one of the “worst” when it comes to cancer.

Insulin, Insulin-like Growth Factor, and Cancer

Insulin is required for the metabolism of carbohydrates—sugars, starches, and cellulose. Dr. Gerald Reaven described what he called syndrome X, later renamed insulin resistance syndrome or metabolic syndrome, which is characterized by low HDL, high triglycerides, and high circulatory insulin levels. Metabolic syndrome involves the combination of central obesity (a.k.a. “pot belly”) and impaired ability to control blood sugar despite higher insulin levels. It has been linked with diabetes and heart disease, as well as cancer.

Insulin receptors occur on both normal and cancer cells. When insulin is secreted from the pancreas in response to dietary sugar, a related substance, an insulin-like growth factor (IGF-1) is secreted by the liver at the same time. Both insulin and IGF-1 activate an important enzyme in cancer cell proliferation called tyrosine kinase.

Colon cancer is strongly associated with metabolic syndrome (Shen Z et al. ANZ J Surg. 2010;80(5):331-6; Aleksandrova K et al. Cancer Prev Res (Phila). 2011;Jun 22). A National Cancer Institute study published in 2003 (JNCI. 2003;95(16):1240-44) showed that obese men also had an almost three-fold increased risk of prostate cancer. Even more alarming is the Physicians’ Health Study, which reported that men with the highest IGF-1 levels had a more than four-fold increased risk of developing prostate cancer (JNCI. 1998;90(12):911-915). Metabolic syndrome and its related elements are also linked to breast cancer, both pre- and postmenopause (Porto LA et al. Arch Gynecol Obstet. 2011;Jan 20. Rosato V et al. Ann Oncol. 2011;Mar 23). Research from the University of Minnesota and the University of North Carolina published in 2008 (Circulation 2008;117:754-761) showed that metabolic syndrome was linked to the consumption of fried foods, diet, soft drinks, and red meat.

Insulin-like growth factor is also a promoter of colon, breast, and prostate cancers. It is made by the liver in proportion to the amount of sugar you consume. However it is also found in the milk of cows that have received genetically engineered bovine growth hormone (rBGH). This is used in the nonorganic dairy industry to stimulate milk production. IGF-1 when consumed in meat usually breaks down in the stomach, unlike IGF-1 consumed in milk. The milk proteins stabilize the IGF-1 so that it is able to be absorbed. One more reason that all dairy products should be organic.

Just how bad is IGF for you? A study published in 2002 by Dr. R. A. Krajcik and colleagues showed that IGF-1 interacts with estrogen to stimulate breast cell growth (Cancer Epidemiol Biomarkers Prev. 2002;11;1566). We have known for years that breast cancer cells have receptors on their surfaces for the IGF molecule, similar to the ones for estrogen. Furthermore, it has been shown that the breast cancer drug tamoxifen can also bind to the IGF receptor and block it, similar to its therapeutic mode with the estrogen receptor. It has been postulated that this is the reason even breast cancer patients without estrogen receptors on the surface can in many cases respond to tamoxifen. Another study published in 1998 showed that premenopausal women with the highest IGF-1 levels had a much higher chance of developing breast cancer than women with average levels (Breast Cancer Res and Treatment. 1998;47(2):111-120).

A 2010 study that followed IGF-1 levels of 633 men over age 50 between 1988 and 1991 found, after 18 years’ follow-up, that men whose IGF-1 levels were above 100 mg/ml at the start of the study were twice as likely to die of cancer as those with lower levels. The increased risk of cancer death for older men with high levels of IGF-1 was not explained by differences in age, body size, lifestyle, or cancer history (Major JM et al. J Clin Endocrine and Metab. 2010;95(3): 1054).

Metformin, a 60-year-old drug for diabetes, has been associated with a 40% reduction in cancer risk. A 2010 study showed metformin inhibits endometrial cancer cell proliferation and is a pro-apoptotic agent (Gynecol Oncol.2010;16(1):92-98). Reducing plasma insulin and IGF levels is also important in decreasing prostate cancer risk (Canc Prev Res. 2008;(5):369-75). Metformin lowers cyclin D1, a growth-promoting protein, as well as depleting prostate cancer cells of ATP (J Lipid Res. 2006;47(10):2306-13). A case-control study of over 900 patients with pancreatic cancer and over 800 controls showed a 62% risk reduction in diabetic patients who had taken metformin compared with those who had not (Gastroenterol. 2009;13(2):482-488).

More than a third of all adults in America today are obese. Women who are obese have a higher risk of postmenopausal breast cancer. Obesity is a risk factor for breast cancer since obesity is associated with high IGF-1 levels, and because fat cells produce estrogens. Estrogens are produced in the ovaries, adrenal gland, and in fatty tissue. As discussed previously, higher estrogens and IGF-1 levels are associated with breast cancer.

Gene-Environment Interaction

It now appears that most cancers do not result from genetic causes. In 2000, the New England Journal of Medicine published the largest study to date on identical twins, who of course share identical genes. Researchers found that these twins developed the same disease only about 10% of the time. Although they did get breast, colon, and prostate cancer between 14 and 30% of the time, this is still a clear indication that something other than heredity is driving cancer rates (NEJM. 2007;343:78-84).

Women with inherited mutations of the tumor suppressor genes BRCA1 and BRCA2 do have an 82% lifetime risk of either breast or ovarian cancer. But recent research has determined that even this has increased since 1940, after which time exposure to environmental carcinogens sky rocketed. The risk was 24% if a mutation carrier was born before 1940, but 67% if she was born later. In the same study, the lifetime risk of ovarian cancer also more than doubled among BRCA1 carriers, and was 23% for BRCA2 carriers (Science. 2003;302:643-646).

Something else is contributing substantially to these cancer risks. Based on much that we have learned in the last 10 years about the adverse interactions between chemicals and genetic makeup, environmental toxin exposure is far and away the most likely culprit. The evidence is overwhelming that something has gone terribly wrong in the last 40 or 50 years—and that it coincides fairly precisely with the vast industrialization and toxic pollution of our world.

Many environmental toxins, such as cadmium, lead, DDT, organochlorine, pesticides, and PCBs markedly promote weight gain. This gives us another clue concerning the parallel rise in the incidence of obesity and cancers related to obesity. It’s no surprise then that a recent study showed pesticide exposure to lab animals caused weight gain—even when caloric intake was decreased. Scientists continuing the search for ways to decrease the effect of tumor-promoting insulin-like growth factors recently published findings in the American Journal of Clinical Nutrition showing that women given 30 mg per day of lycopene in supplemental form had about a 20% increase in the binding protein for insulin-like growth factor (2007;86(5):1456-1462). Such binding proteins can reduce the effect of hormones like estrogen and tumor promoters like Insulin like growth factor.

While a genetic susceptibility may combine with a chemical to create the disastrous effects we’ve been discussing, the fact is that without the chemical, the genetic susceptibility might well lie undiscovered for a lifetime. We have to ask ourselves two basic questions: “What is a safe level of exposure to these carcinogens?” and “Is there a safe level for pregnant women and developing fetuses?”

More than 10 years ago, the National Cancer Institute answered the first question. Its answer in 1990 was “None.” In an NCI booklet called, “Everything Doesn’t Cause Cancer,” the Institute said, “There is no adequate evidence that there is a safe level of exposure for any carcinogen…. Low exposure that might be safe for one person might cause cancer in another.” Since there is no method that can measure any one person’s individual risk, the Institute concluded, “Exposure to a low level of a carcinogen thus has to be considered a risk for everyone.” More than 20 million Americans are exposed to toxic chemicals every year in concentrations that are at least 100 times greater than the EPA deems “acceptable levels.” These compounds continue to be overused and underregulated, both here and in much of the industrialized world. As U.S. Assistant Surgeon General David Rall has reported, every single chemical known to cause cancer in humans is also known to cause cancer in experimental animals.

Two studies about a common food-based substance called acrylamide demonstrate just how pervasive and harmful these environmental chemicals can be. In 2007, Janneke Hogervorst and colleagues noted that high dietary intake of acrylamide could raise the risk of endometrial cancer by 29% and the risk of ovarian cancer by 78% (Cancer Epidemiol Biomarkers Prev. 2007;16:2304). You may be asking “What in the world is a acrylamide?” Acrylamide is a carcinogen created when high-starch foods are baked, toasted, or roasted like those crunchy chips you may consume with snacks or lunch. Cigarette smoking also generates large amounts of acrylamide. Even more concerning is a 2008 study from Denmark published in the International Journal of Cancer that measured blood levels of acrylamide in women with and without breast cancer. The study found that women with the highest levels of acrylamide were twice as likely to develop breast cancer as women with the lowest levels (Int J Cancer. 2008; 122:2094-2100).

Other studies have illustrated that most of us have been exposed to and are currently carrying measurable levels of endocrine disrupting chemicals (EDCs), ranging in total numbers from the tens to the hundreds of different ones. While these EDCs remain undetected in any routine medical checkup, they alter reproductive hormones in humans, as they do in wildlife. The problem is that most of us don’t know we are carrying them, which makes it extremely difficult to determine the amount of exposure, and even harder to determine sources. That is why biological samples are so critical in researching these toxins.

 Why choose organic food?

• Nutritional content
• A meta-analysis reported that vegetables grown without pesticides may have significantly more antioxidants than conventionally grown vegetables (J Alt Health Comp Med. 2001;7(2):161-173).

• A survey of the literature comparing nutrient content of organic and conventional crops, which used published comparative measurements of organic and conventional nutrient content entered into a database for calculation, found that organic crops contained significantly more vitamin C, iron, magnesium, and phosphorus and significantly less nitrate than conventional crops (J Altern Complement Med. 2001;7(2):161-73). Some of the original data was presented 2/23/95 by J.B. Pangborn and B. Smith at the 13th Annual International Symposium on Man and His Environment in Health and Disease, Dallas, TX (cited by Dr. William Rea at IFM International Symposium 4/20/06).
• Statistically higher levels of total phenolics were consistently found in organically and sustainably grown foods (blackberries, corn, strawberries) as compared to those produced by conventional agricultural practices (J Agric Food Chem. 2003.  51 (5). 1237 -1241).
• Higher levels of polyphenols were found in organically grown peaches (Food Chem. 2001. 72. 419-424).
• There have been negative findings on nutrition comparisons. A systematic review identified 162 studies using one of three designs: field trials (comparing adjacent parcels of land), farm surveys (comparing products from organic and conventional farms), and basket studies (comparing foods available through retail outlets). The authors examined 11 nutrient categories reported in at least 10 studies (vitamin C, phenolics, magnesium, potassium, calcium, zinc, copper, total soluble solids, titratable acid, phosphorus, and nitrogen) or at least 4 livestock studies (ash and unspecified fats). The only differences were that conventional crops contained more nitrogen whereas organic crops contained more phosphorus and titratable acid, and these differences might be due to differences in ripeness or fertilizer use (Dangour AD, et al. Am J Clin Nutr. Epub 7/29/09). The studies identified, however, were thought to be heterogenous and often of poor quality (Greenfield RH. Commentary. Alt Med Alert. 2009;12:97-99).

• Safety

• A longitudinal 15-day study in Seattle, in 23 children ages 3-11, concluded that dietary intake of pesticides represents a major source of exposure for infants and children and that an organic diet provides a dramatic and immediate protective effect against exposure to commonly used organophosphate pesticides, which are known to cause neurological effects in some humans (Environment Health Perspect at http://dx.doi.org/ and reviewed in Alt Med Alert. 2006;9:11-12).
• The list of nonorganic crops that are most likely to be contaminated with pesticides varies over time. The Environmental Working Group periodically updates its list of “dirty dozen” fruits and vegetables most contaminated with pesticides; for an updated list, go to http://www.foodnews.org/, click on Food News from the Environmental Working Group, and scroll to the bottom of the page for a ranking of fruits and vegetables with the most to the least amount of pesticide residue. This list is periodically updated.
• There is dangerous synergy in these compounds. For instance, a Tulane study showed that when 2 pesticides, dieldrin and endosulfan, were combined, the estrogenic effect of each dramatically increased (Env Health Perspect. 1996;104(10):1020-1023).
• We’ve seen red meat labeled “antibiotic and hormone free” in the freezer sections of our local supermarkets, but is it better? Apparently so. Studies investigating zeranol, a growth hormone used in cattle, veal, and lamb, have shown that “contamination of food by zearalenone and its natural metabolites (breakdown products) has been associated with the development of precocious puberty—a known risk factor for breast cancer—in young girls (Massart F et al. J Perinatol. 2005;25:282-288). These compounds have also been shown to enhance proliferation of ER+ human breast tumor cells in vitro through estrogen-mediated pathways and activation of gene profiles similar to those activated by the natural hormone estradiol (Khosrokhavar R et al. Toxicol Mech Meth. 2009;19:246-25; Parveen M et al. FEBS Lett. 2009;583: 2377-2384).
• DDT provides another cautionary example. It was sprayed on crops in the U.S. from 1950 to the early 1970s, despite evidence of harm as early as 1951. It was not banned until 1972. DDT is deposited in breast tissue. DDT, like other toxins, has been linked to breast cancer. It works its way up the food chain in a process called bioaccumulation. DDT mimics estrogen and breaks down in the body to DDE. A Danish study comparing women with breast cancer to those without, found women with the highest levels of DDE had a 300% higher risk of breast cancer (Cancer Causes Control. 2000;11(2):177-184). DDT is still sprayed in many other countries and comes into the US as out-of-season produce.

Additional references on nutrition and safety in organic foods:

• Brandt K, Leifert C, Sanderson R, Seal CJ. Agroecosystem management and nutritional quality of plant foods: the case of organic fruits and vegetables. Crit Rev Plant Sci. 2011;30(1):177-197.
• Hunter D, Foster M, McArthur JO, et al. evaluation of the micronutrient composition of plant foods produced by organic and conventional agricultural methods. Crit Rev Food Sci Nutr. 2011;51(6):571-582.
• Lairon D. Nutritional Quality and Safety of Organic Food. In: Lichtfouse E, Hamelin M, Navarrete M, Debaeke P, eds. Sustainable Agriculture Volume 2: Springer Netherlands; 2011:99-110-110.
• Worthington V. Nutritional quality of organic versus conventional fruits, vegetables, and grains. The J Altern Compl Med. 2001;7(2):161-173.
• Zhong S, Ye WEIP, Feng E, et al. serum derived from zeranol-implanted aci rats promotes the growth of human breast cancer cells in vitro. Anticancer Research. 2011;31(2):481-486.
• Ye W, Xu P, Jen R, et al. Zeranol down-regulates p53 expression in primary cultured human breast cancer epithelial cells through epigenetic modification. Int J Molec Sci. 2011;12(3):1519-1532.

Inflammation and Cancer

Prostaglandins, a team of hormone like substances that affect immune response and blood pressure, can inhibit certain allergies, and depending on the prostaglandin, provoke or prevent inflammation.  PGE-1 is important in protecting your stomach from too much acid and keeping your kidneys working normally, among other things. This is why people who take too much aspirin can occasionally develop problems with ulcers and kidney disease.

Many spices can inhibit prostaglandins. The best method of lowering PGE-2 is usually to inhibit levels of the COX-2 enzyme, which can often be done by consuming the omega-3 fatty acids found in fish, plankton, flaxseed, and hempseed.

Rosmarinus officinalis is a member of the mint family (Lamiaceae). It can grow to 5 feet tall and remain in the same place for up to 30 years if taken well care of. Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as an antioxidant and anticarcinogen. Rosemary helps protect against the initiation of breast tumors. It is a potent inducer of detoxification enzymes. Hence, it is no surprise that a study in rats that were given rosemary before ingestion of breast-cancer–inducing toxins found that they developed almost 75% fewer breast tumors than rats not pretreated with rosemary (Cancer Letters. 1996;104(1):43-48). Rosemary (like green tea) has also been found to increase the concentration of chemotherapeutic drugs in breast cancer cells.

In Russia, garlic is compared to penicillin, and extracts have been used for its great antimicrobial and antifungal power. During both World War One and World War Two, medics would use garlic to disinfect war wounds. Evidence has shown garlic to be a natural form of cancer prevention. Studies using garlic tablets in vitro also showed an increase in natural killer cell activity. (German J Oncol. 1989;21:52-53). A meta-analysis of studies done between 1966 and 1999 also revealed that people who consumed fresh or cooked garlic daily were 40% less likely to develop colorectal cancer and the risk of gastric cancer was reduced by 47% (Am J Clin Nutr. 2000;72(4):1047-1052).

In the case of cancer prevention, turmeric can help keep metastases at bay. Curcumin in turmeric slows the growth of tumor cells and keeps cancer cells from replicating (J Ethnopharmacol. 1994;44(3):211-217). Studies are also under way to see if curcumin can cut off the oxygen supply tumor cells require in order to survive.

Turmeric has great anti-inflammatory properties that make it a natural aid for various forms of arthritic conditions. It has been shown to suppress the biological enzyme cyclooxygenase-2 (COX-2), thereby reducing the production of prostaglandins involved in causing painful inflammation. Reducing COX-2 is of great importance in inflammation because it is directly related to cancer formation; cyclooxygenase is known to have a central role in tumorigenesis.

A 2011 study showed people who took aspirin at least once a month were 29% less likely to develop pancreatic cancer as those who did not (American Association for Cancer Research, 102nd Annual Meeting, 2011). A 2010 study of >4000 breast cancer survivors showed that those who took aspirin had a 50% lower risk of dying from breast cancer and a 50% lower risk of metastatic disease (J Clin Oncol. 2010;20(9): 1467-1472).

The nutritional agents I believe should be studied are combinations of extracts from green tea, black raspberry, pomegranate, rosemary, turmeric, maitake, shitake, and brown seaweed.

Types of Fat and Cancer

Premenopausal women who eat more than one and a half servings of red meat per day had double the risk of estrogen receptor positive breast cancer compared to women who eat less than three servings per week, according to the Harvard Nurses’ Health Study published in the Archives of Internal Medicine (2006;166:2253-2259). I believe the high saturated fat intake as well as carcinogenic heterocyclic amines present in cooked and processed meats account for these findings. Harvard researchers updated their results of the Physicians’ Health Study and presented the data at the 2006 American Association for Cancer Research meeting. The study showed men who ate fish at least five times per week reduced their chance of developing colorectal cancer by 40%. The COX-2 inhibitory effect of fish oil was presumed to play a role.

Polyunsaturated fats come in three forms: omega-3, omega-6, and omega-9 fatty acids. The omega-3s are found in cold-water fish like salmon, sardines, halibut, cod, and tuna, as well as vegetables like flaxseed, hempseed, and walnut oils. One of the main constituents of flaxseed is alpha-linolenic acid. A study published in the 1994 British Journal of Cancer showed that breast cancer patients with low levels of alpha-linolenic acid in breast tissue had an increased risk of developing metastatic disease (Br J Can. 1994;70(2):330-334). Conjugated linoleic acids (CLAs), unlike other omega-6 fatty acids, lower the risk of breast cancer by reducing estrogen and promoting lower body fat and lean-muscle mass. Since fat cells produce estrogen, the presence of more muscle and less fat lowers estrogenic initiation of cancer. In addition, a study published in 2000 in Nutrition and Cancer showed women with the highest CLA levels had significantly lower rates of breast cancer (2000;38(2):151-157). CLAs are found so minimally in our diet that supplements are necessary to benefit from those fats.

CLAs have been documented to inhibit cancer cell growth and protect against environmental toxins initiating breast cancer. Another study in the British Journal of Cancer demonstrated that breast cancer rates consistently fell with increased fish consumption and rose with increased animal fat (2003;89:1672-1685). A 1995 study in Nutrition and Cancer showed that women who developed breast cancer had significantly lower levels of EPA and DHA, the two omega-3 fatty acids in fish (1995;24(2):151-160). Omega-3 fatty acids are beneficial in decreasing the activity of the COX-2 enzyme which promotes inflammation. In addition, they have been found to decrease estrogen stimulation of breast cell growth. 

Flaxseeds contain the highest levels of omega-3 fatty acids of any vegetarian source. Can an omega-3 fatty acid fish oil supplement increase tissue levels in humans? Can the supplements actually suppress the inflammatory COX-2 enzyme in humans? The answer to both questions, according to an April 2008 paper published in the American Journal of Clinical Nutrition (2008;87(4):949-956), is a resounding yes. Researchers from the Norfolk and Norwich University Hospital and the Institute of Food Research studied patients with Barrett’s esophagus (a condition caused by acid reflux in which the lining of the esophagus shows precancerous changes). Half the patients were given 1500 mg of the omega-3 EPA supplement, and half were not. At the end of the study biopsies of the esophagus were obtained. The EPA-treated group had not only higher levels of omega-3 fatty acid in their cells, but COX-2 protein significantly decreased in the tissues of the omega-3 supplemented group.

To summarize, the two best fats are (1) omega-3 fatty acids, which lower the risk of breast cancer by increasing detoxifying enzymes, lowering inflammation, and reducing the rate of breast cell proliferation in response to estrogen; and (2) CLA (conjugated linoleic acid).

The worst fats are trans fats, which are formed by the hydrogenation of vegetable oil used to make processed foods harder and extend their shelf life. A 2008 study published in the American Journal of Epidemiology (2008;167(11):1312-1320) followed almost 20,000 women over 7 years and found those who consumed the most trans-fatty acids had a 75% increased risk of breast cancer. My advice is to never consume any products containing these fats.

Women’s Health Eating and Living (WHEL) Study

The Women’s Health Eating and Living (WHEL) Study was a randomized trial assessing whether a dietary pattern very high in vegetables, fruit, and fiber and low in fat reduces the risk of recurrent and new breast cancer and overall mortality among women with previously treated early-stage breast cancer (Controlled Clin Trials. 2002;23(6):728-756). Previous studies have shown differing associations between prevention of breast cancer recurrence and a diet high in vegetables and fruit and low in total fat. The WHEL Study set out to explore this relationship in a cohort of 3,088 women, who were aged 18 to 70 when initially diagnosed with early-stage breast cancer.

The WHEL Study was a randomized trial that provided for a control group and an intervention group. The intervention group received telephone counseling about diet, supplemented with cooking classes and newsletters that promoted the recommended daily servings of fruit, vegetables, fiber, and fat. During the study follow-up period of just over seven years, the intervention group maintained statistically significant differences in their diet from the control group. They consumed many more vegetables, fruits, and fiber; and a much smaller percentage of their energy intake came from fat. However, during the follow-up period, the researchers found that the intervention and control groups had no difference in breast cancer events or mortality. With recurrence rates of 16.7% in the intervention group and 16.9% in the control group, no significant difference in breast cancer recurrence rates was observed.

The data seem to suggest that a diet high in fruits and vegetables and low in fat is not associated with improved breast health outcomes in women who previously have been treated for early stage breast cancer. However, breast cancer takes decades to develop and a seven-year limited intervention might not show improvements similar to those found in primary prevention studies.