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The four-day event (May 20–23, 2010) provided a wide range of information to an audience of healthcare professionals from 21 different countries. The large international interest may be indicative of a growing global interest in functional medicine and innovative thinking surrounding integrative oncology.

During her presentation, Mary Hardy, MD, medical director for the Simms/Mann–UCLA Center for Integrative Oncology, told the audience that patients with cancer visit the doctor twice as often as other patients. She explained that the primary care physician (PCP) often takes a step back during cancer treatment; however, there is a need for PCPs to step forward and play a more active role with their cancer patients.

Hardy, who was on the development panel for the symposium said, “Our goal was to empower IFM/IM primary care physicians to do the things they already know how to do well. This will give the cancer patient the best blend of conventional and complementary care leading to the best outcomes and least toxicity.”

The focus of the symposium was to view cancer as a chronic disease and then address issues associated with the care and healing from this illness. Some key topics included

• oncogenetic expression;
• genetics, epigenetics, and environment;
• antioxidants;
• confusion about vitamin D;
• diet and lifestyle;
• offsetting side effects of conventional treatments; and
• enhancing conventional treatments via an integrative approach.

This is the first time that the Institute for Functional Medicine tackled the issue of cancer care in one of its symposia. “This conference really brought together some of the best clinical practitioners in integrative oncology,” said Tina Kaczor, ND, FABNO, senior medical editor of the Natural Medicine Journal, who also attended the symposium.

“I was pleased to see that several of my colleagues who are Fellows of the American Board of Naturopathic Oncology— specifically Lise Alschuler, Tim Birdsall, Paul Reilly, and Dan Rubin—were speakers at this event,” said Kaczor. “I think naturopathic oncology has a lot to offer in terms of focusing on the patient and using natural agents that benefit our patients throughout their course of treatment. Our education makes us uniquely positioned to understand and integrate various modalities to improve each patient’s quality of life, as well as affect their risk of recurrence.”

Each morning of the symposium Bland provided a synthesis of the information presented the day before. This snapshot not only added Bland’s perspective to the various topics, it also neatly encapsulated points of interest and appeared to be well received by the audience. “This was the class I wish I had available to me years ago when I was struggling to learn how to support cancer patients,” Hardy concluded.

One of the highlights of the symposium was the presentation of the Linus and Eva Helen Pauling award to Dean Ornish, MD, who was also a presenter at the symposium. “Dean Ornish was the first to see that treating the underlying metabolic and nutritional causes of disease was more powerful than conventional medical and surgical approaches to chronic disease,” explained Mark Hyman, MD, who presented Ornish with the award. “Receiving the 2010 Linus Pauling Award is recognition of his seminal contribution to the field of nutritional and functional medicine.”

The United States Census Bureau projects that between 2000 and 2030 the number of Americans 65 years old or older will double. The aging of our population, combined with many other factors, will likely contribute to a corresponding increase in serious illnesses such as cancer. In fact, it is now estimated that 1 in 2 men and 1 in 3 women will develop cancer in a lifetime. Concurrently, an increasingly high number of individuals are living beyond their prognosis. In 2007, more than 11.7 million people were living with a history of cancer.

Cancer continues to put a strain on our healthcare system, not only in terms of increasing prevalence but also increasing costs per individual. A recent report published online in the journal Cancer indicated that the cost to treat cancer has nearly doubled in the past 20 years.

Additionally, if we remain on this course, the number of people diagnosed with cancer will soon far outweigh the number of oncologists available to treat them. Additionally, if we remain on this course, the number of people diagnosed with cancer will soon far outweigh the number of oncologists available to treat them. Data from Erickson and colleagues published in 2007 pointed to a projected shortage of more than 4,000 oncologists by the year 2020.5 The conclusion based on the data was that “a multi-faceted strategy will be needed to ensure that Americans have access to oncology services in 2020. … Among the options to consider are increasing the number of oncology fellowship positions, increasing use of non-physician clinicians, increasing the role of primary care physicians in the care of patients in remission, and redesigning service delivery.”

Primary care physicians may be able to fill some of the gaps now emerging in cancer care. Primary care physicians can help manage side effects and after effects of conventional treatment, counsel patients on diet, and provide practical lifestyle advice that can enhance survivorship and help prevent a recurrence. As it turns out, the increasing prevalence of cancer as a chronic disease provides an increasing opportunity for the primary care physician. This could also be good news for the patient. For example, preliminary research shows that utilization of primary care in the early phase of lung cancer treatment reduced mortality risk.

The 17th International Symposium on Functional Medicine was designed to engage the primary care community in integrative cancer treatment. In his opening presentation, Jeffrey Bland, PhD, FACN, CNS, who founded the Institute for Functional Medicine with his wife Susan, asked the question “How can we deliver better care to our patients?” To a sell-out crowd of doctors, nurses, and other healthcare professionals, featuring a large number of primary care providers, Bland and the other expert presenters attempted to teach how functional medicine can play a role in cancer care. “We need to look at the soil in which these oncogenes can grow,” says Bland. “For many patients, cancer has become a chronic disease that demands long-term management.”

A major limitation of this sero-epidemiological study is based on the fact that fatal prostate cancer takes many years from formation until death occurs. The question is whether the fatty acid content of a man’s blood on two days out of the thousands of days over those years is a reliable measure of his average fatty acid status. Another limitation is that the researchers did not take into account the impact of vitamin E, selenium, lycopene, cruciferous vegetables, meat and dairy intake.

EPA and DHA are hypothesized to reduce cancer risk in general through their anti-inflammatory and immunomodulatory properties, and by affected cell permeability, gene expression, and signal transduction. The effects of omega-3s on these pathways in prostate carcinogenesis are not fully understood. There is no known mechanism by which EPA or DHA would be procarcinogenic, nor is there any evidence suggesting anticancer properties of trans-fats.

Genetic and molecular studies of high-grade prostate intraepithelial neoplasia have indicated that loss of heterozygosity is prominent and that certain oncogenes are expressed. What causes the expression of these oncogenes? What downregulates their expression?
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Androgenic hormones are necessary for prostate growth and development. It is not surprising that polymorphic variants of genes involved in androgen action may affect PCa risk. African Americans, who have higher PCa risks than Asians, have androgen-receptor polymorphisms that result in their increased predisposition. 5-alpha reductase variants also may respond differently to inhibition by finasteride.

The key lifestyle factor in the United States most likely responsible for high PCa incidence is the diet, generally rich in animal fats and meats and poor in fruits and vegetables.
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Accumulated epidemiologic evidence implicates the environment as the major contributor to the development of most prostate cancers. PCa incidence has wide geographic variation, with high rates in the US and Western Europe and low rates in Asia. African Americans have very high PCa risks. The geographic variation can be explained best by lifestyle, as Asian immigrants to North America have higher PCa risks. The key lifestyle factor in the United States most likely responsible for high PCa incidence is the diet, generally rich in animal fats and meats and poor in fruits and vegetables. Total fat intake, animal fat intake, and consumption of red meats are associated with increased PCa risk.3 Ingestion of 2-amino-1-methyl-6-phenylimidazopyridine, one of the hererocyclic amine carcinogens that appear in “well-done” red meats, leads to PCa in rats. Consumption of dairy products also increases PCa risk.

Consumption of lycopene, cruciferous vegetables, vitamin E and selenium reduce PCa risk.
The role of genetics in identifying individuals at high risk for prostate cancer are in their infancy, but epidemiologic studies support the concept that genetic risk plays a role, and clinical studies support the observation that early prostate cancer in some individuals is highly aggressive, while in the majority it is indolent. Linking these two factors should identify a population of men in whom screening, early detection, and chemoprevention agents can be intensively directed. In the meantime, the take-home message of this study was expressed by the chief author: “Overall, the beneficial effects of eating fish to prevent heart disease outweigh any harm related to prostate cancer risk.”

Design
A 7-year, randomized, placebo-controlled trial that tested whether the 5 alpha-reductase inhibitor, finasteride, reduces prostate cancer (PCa) risk. Over the course of the study, men underwent annual prostate-specific antigen (PSA) and digital rectal examination (DRE) testing. Men who had an abnormal DRE or PSA>/= 4.0 ng/mL were recommended for prostate biopsy. At the end of the study, all men who had not been diagnosed with PCa were requested to undergo a prostate biopsy.

A case-control study was nested within the Prostate Cancer Prevention Trial. Serum phospholipid levels were compared from 1,809 men with biopsy-confirmed invasive prostate cancer and 1,809 men (controls) who were disease-free at the end-of-study biopsy. Controls were frequency matched to cases on distributions of age (+/- 5 years), treatment group (finasteride/placebo), and a first-degree relative with PCa, and they were oversampled for nonwhites.

Participants
18,882 men age 55 or older were randomized to receive finasteride or placebo.
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Study Medication
Subjects received finasteride 5 mg/day.

Outcome Measures
Serum samples were collected at years 1 and 4 and pooled to reduce intraindividual variability of the phospholipid fatty acid assay. Calculations were made of eicosapentaenoic acid (EPA) + docsahexaenoic acid (DHA) as a measure of total long chain omega02 fatty acids; linoleic + arachidonic acids as a measure of total omega-6 fatty acids; total trans-fatty acids (TFA) 18:1; total TFA 16; and total TFA 18:2.

The primary outcome measure was the distribution of serum phospholipid fatty acids by percent of total among PCa cases and controls, stratified by prostate cancer grade.

Key Findings
Levels of DHA were higher among high-grade cases compared with controls. Levels of TFA 18:1 and 18:2 were significantly lower among high-grade cases compared with controls. There were no other significant differences of the remaining phospholipids between control and cancer groups. EPA was not associated with risk of high-grade PCa, and associations were similar for EPA+DHA to that of DHA alone.

Practice Implications
Epidemiologic, animal model, and in vitro studies indicate that omega-3 fatty acids, lycopene, and selenium are chemopreventive for PCa. The findings of this study run counter to what the investigators hypothesized, which was that omega-6 and TFAs would be positively and omega-3 fatty acids inversely associated with PCa risk. Although unexpected, the authors cite several other studies that are consistent with their results, and the possibility exists that there may be an inverse association of fish consumption with late stage or fatal prostate cancer. It is important to keep in mind, however, that it was only DHA, and only high-grade prostate cancer, where an increased risk of PCa risk was found. Replication in more studies is needed before any conclusive recommendations can be made.

Design
Forty-six patients with a diagnosis of non-small cell lung cancer (NSCLC) completed the study. All patients received a standard first line chemotherapy regime (carboplatin with either vinerelbine or gemcitabine). The standard of care (SOC) arm (n=31) received only the chemotherapeutic agents; the fish oil (FO) arm (n=15) consumed 2.5 grams EPA/DHA per day in addition to their chemotherapy. Study duration was one year.

Outcome Measures
Assessments were made using imaging and clinical examination. Measures included response rate (complete response + partial response) and clinical benefit (complete response + partial response + stable disease divided by the number of patients).
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Key Findings
Overall favorable response rate in the FO group was more than double that of the SOC group (60% vs. 25.8%, P= 0.008). Clinical benefit was also higher in the FO group vs. SOC group (80% vs. 41.8%, P= 0.2). There was a trend toward improved survival at the 1-year point in the FO group as well (60% vs. 38.7%, P= 0.15). Lastly, dose limiting toxicities did not differ between the two groups (P=0.46).

Clinical Implications
Previous studies in vitro and in vivo have shown omega-3 fatty acids may increase the cytotoxicity of chemotherapy agents.1,2 While such preliminary evidence points to potentiation of chemotherapy, there is little clinical trial data to date to substantiate these claims. The current abstract strengthens the body of evidence that suggests EPA/DHA may sensitize cancer cells to the cytotoxic effects of chemotherapeutics. It is also the first to demonstrate this effect in NSCLC patients specifically.

While this study used a platinum-based chemotherapeutic and either gemcitabine or navelbine, the effect may not be dependent on the specific chemotherapy agents used. There was a phase II study of metastatic breast cancer patients receiving anthracycline based chemotherapy and 1.8 grams/day of DHA from an algal source. Dosing began 7–10 days before the start of chemotherapy and continued throughout. In addition to overall survival, this study assessed DHA incorporation into phospholipids and found that incorporation varied greatly between individuals. Only those considered “high incorporators” had an increase in overall survival.3 One hypothesis of how omega-3 fatty acids may potentiate cytotoxic agents is through increasing the oxidative potential of the phospholipid bilayer. Increased overall survival only in those womenwho were “high incorporators” of DHA supports this hypothesis.

This bolsters the case for inclusion of omega-3 fatty acids in all patients with NSCLC undergoing chemotherapy.
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Earlier studies in rodents suggested DHA may convert chemo-resistive mammary tumors to chemosensitive and radiosensitive tumors. The chemosensitization was nullified when alpha-tocopherol was given concomitantly, again supporting the role of lipid peroxidation as the mechanism of action. Other mechanisms of chemosensitization that have been proposed include influencing signaling proteins such as Ras, Akt, and Her2neu, altering expression or function of apoptotic proteins, affecting survival factors such as NF-KappaB, or increasing drug uptake or activation.5

It should be noted that the best-evidenced use of fish oil supplementation in integrative cancer care is not for chemo-sensitization but as an anti-cachectic agent.6 In regard to lung cancer specifically, one study showed that patients with sarcopenia (muscle wasting) have significantly less plasma EPA, DHA, and total fatty acids after 2.5 months of chemotherapy. Another study of patients with lung cancer given fish oil in supplement form showed improved appetite, less fatigue, and lowered C-reactive protein. In a separate publication, the authors of the current abstract showed that muscle mass was better preserved in NSCLC patients who consumed 2.2 grams of EPA//DHA during treatment versus those just receiving standard of care. While preservation of muscle mass is enough reason to recommend supplementation with EPA/DHA in NSCLC patients, the current study suggests response rates and overall survival may also benefit. Certainly, this bolsters the case for inclusion of omega-3 fatty acids in all patients with NSCLC undergoing chemotherapy.

Study Limitations
This is a small study of only 46 participants. Nonetheless, it did reach statistical significance. There was no placebo used in the group that did not take fish oil. A placebo control would strengthen the findings considerably, as it is possible that those patients healthy enough to swallow addition pills would be expected to have longer survival as well.

Key Findings
Drinking two or more sodas a week almost doubles a person’s risk of developing pancreatic cancer. Following these people for 14 years yielded 648,387 person-years of data and 140 cases of pancreatic cancer (PC). Individuals who consumed 2 or more soft drinks a week experienced a statistically significant increase in risk of pancreatic cancer (hazard ratio, 1.87; 95% confidence interval, 1.10–3.15) compared with individuals who did not consume soft drinks. There was no association seen between drinking fruit juice and risk of PC.

Practice implications
This is just the latest in a series of studies on the subject that have yielded sometimes conflicting and confusing results. Yet the bottom line consensus appears to be that soda or other concentrated forms of sugar, such as candy bars, do increase risk of pancreatic cancer.

Pancreatic cancer does not respond well to treatment: 5-year survival even with modern treatment is less than 5%. Therefore, prevention is the best approach. Cigarette smoking is the one accepted risk factor consistently associated with increased risk of pancreatic cancer. Type 2 diabetes also increases risk, which led to a theory that producing high levels of insulin might somehow lead to malignant transformation of pancreatic cells.

In most cancers, the cells that become cancerous have been somehow overworked, irritated, or in some way abused before becoming cancer cells. They have been pushed by something to grow faster, work harder, secrete more or in some manner live harder lives. Estrogen pushes both breast and uterine cells to become cancerous. Testosterone pushes prostate cells to become prostate cancer. Infections push lymph cells to become lymphoma. This theory about pancreatic cancer suggests that high sugar intake pushes the pancreas.

Diabetes has been associated with pancreatic cancer for decades. A study on Seventh Day Adventists published in 1988 reported that “prior history of diabetes was associated with increased risk of subsequent fatal pancreas cancer.”1

A Kaiser Permanente study published that same year found that while cigarette smoking increased risk of pancreatic cancer by a factor of 2.5, people who had been treated for diabetes had 4.5 times the risk. (Smoking: relative risk, 2.5; 95% confidence interval, 1.3–4.7. Diabetes: relative risk, 4.5; 95% confidence interval, 1.2–16.7)2

A Dutch paper published in 1990 that analyzed data on 164 patients with pancreatic cancer found “a significant, positive association between pancreatic cancer and past habitual intake of simple sugars.” (OR 1.95; 95% confidence interval, 1.24–3.07). This led the study authors to suggest that “the development of exocrine pancreatic carcinoma is positively related to past habitual intake of total energy, total carbohydrates, and simple sugars.”3

A 1991 Australian paper that analyzed the habits of 104 people who developed PC also found a link to sugar consumption. “For the top quartile of refined sugar intake, the estimated relative risk was 2.21 (95% confidence interval, 1.07–4.55).”4

A December 1995 study that looked at 179 cases of PC in French speaking Canadians found a similar effect of sugar consumption. Again, high sugar consumption nearly tripled risk. Of interest in this paper was the pronounced effect of cooking with firewood, a habit that increased relative risk by a factor of almost 5, while cooking in a pressure cooker lowered risk to one-third the average.5

Sweetened carbonated drinks, what we call soft drinks, or soda, are a major source of simple sugars in western diets. As such, soda consumption provides a measure of overall sugar consumption.6 Soda consumption is associated with hyperglycemia and hyperinsulinemia, obesity, and type 2 diabetes.

Rates of developing pancreatic cancer have plateaued and are stable in the United States, but they are rising among Chinese men and women in Singapore. From 1968 to 1998, they have almost doubled (going from 3.7 to 5.4 per 100,000 for men and 1.5 to 3.4 per 100,000 for women). One explanation for this increase is the shift toward a more western diet and increased consumption of sugar and sugar-sweetened sodas. It may be that during this transition period between traditional diets and western diets, the effect of soda consumption is more pronounced. Soda may be adopted into the diet while traditional foods and recipes still comprise the basic diet.

Design
Statistical mining of data collected on dietary habits of women with breast cancer. Diet in the 12–24 months before diagnosis was assessed with an extensive food frequency questionnaire, and confounders assessed from an epidemiologic interview and abstracted clinical data. Lignan intake was calculated using published food composition data.
Participants: 1,122 women, aged 35–79 years, diagnosed with breast cancer between 1996 and 2001. Data were collected as part of a study looking at lifetime alcohol consumption and breast cancer (WEB Study).

Study Methodology
The association between dietary lignan intake and survival was analyzed. Vital Status was tracked until the end of 2006. Extensive food questionnaires were used to track diet for 1–2 years before initial diagnosis. Lignan intake was calculated using current food composition tables. Hazard ratios (HR) for dietary lignan intake with all-cause and breast cancer mortality were calculated.

Outcome Measure
Vital status (living or deceased)

Key Findings
Postmenopausal women who consumed the most lignans had a significantly lower risk of dying from any cause and especially from breast cancer than women who ate only small amounts of lignan-containing foods. When upper versus lower quartiles of lignan intake were compared, there was a 51% (HR 0.49, 95% CI: 0.26–0.91) reduction of all-cause mortality in those consuming the higher lignan levels. These women had a 71% decreased risk of dying of breast cancer (HR 0.29, 95% CI: 0.11–0.76). High intakes of dried beans (HR 0.61, 95% CI: 0.36–1.03) may have also lowered risk of overall mortality and breast cancer mortality (HR 0.53, 95% CI: 0.24–1.14), though these numbers did not reach statistical significance.

Practice Implications
This is the first paper to examine the association of lignan intakes prior to breast cancer diagnosis and risk of dying. These findings suggest that we should actively promote consumption of lignan-containing foods, particularly in postmenopausal women.

Participants
158 total subjects (44 with pancreatic adenocarcinoma, 42 with gastric adenocarcinoma, 40 with gallbladder adenocarcinoma, and 32 with hepatocellular carcinoma); 25% were diagnosed with stage III and 71% with stage IV disease.

Inclusion criteria:
histopathology/cytopathologic confirmation of malignancy,
inoperable tumors, and
no prior chemotherapy or radiation treatment.

Treatment
Psorinum 6X was administered, up to 0.02 ml/Kg body weight orally (as liquid drops under the tongue) once daily for all participants. Conventional (eg, infection and pain control, electrolyte balancing, abdominal/pleural paracentesis) and homeopathic (ie, administration of homeopathic medicines on pathological indications) supportive measures were also administered.

Results of this study, which demonstrate a 19-38-fold improvement compared to conventional treatment in five-year survival of non-resectable pancreatic cancer are, to put it mildly, intriguing.

Outcome measures
Primary outcome measures were radiological tumor response and survival at 1, 2, 3, 4 and 5 years. Secondary outcome measure was assessment of side effects of Psorinum 6X.

Key Findings
Complete tumor response occurred in 33.33% of those diagnosed with stage III disease and 10.71% of those with stage IV. Partial response occurred in 41.03% and 33.93% respectively.

Five-year survival rates were 38.64% (pancreatic), 38.1% (gastric), 37.5% (gallbladder), and 43.75% (liver).

No adverse effects of Psorinum were observed, though a few participants had mild oral irritation and skin itching.

Clinical Implications
The cancer types considered in this study are among the most intractable and deadly malignancies. Conventional treatment of these conditions, though improving, is still of very limited effectiveness. For instance, in the last decade with the use of the standard first-line therapy gemcitabine, median overall survival for advanced pancreatic adenocarcinoma has increased from 3–4 months to 5–8 months,1 while 5-year survival of the non-resectable form is nearly unchanged at a dismal 1–2%.2,3 Roughly 80% of all pancreatic malignancies are inoperable at diagnosis.4 Therefore, results of this study, which demonstrate a 19–38-fold improvement compared to conventional treatment in five-year survival of non-resectable pancreatic cancer are, to put it mildly, intriguing.

Similar improvements in survival rates with Psorinum therapy were demonstrated in the other cancer types studied.

Caution should be taken, however, in interpreting these findings. Promising phase II trials are notorious for disappointing in the phase III setting. Independent verification in a controlled context is needed before an unqualified recommendation can be made.

Nevertheless, considering the very poor response of these cancers to conventional treatment and the apparent lack of toxicity and potential benefit of Psorinum therapy, it seems reasonable that clinicians with oncologic experience might offer this therapy to their patients on an individual basis.

Common homeopathic medicines such as Lycopodium 200C and Baryta carbonicum 200C were used supportively and prescribed on a pathologic (as opposed to individualized) basis. This is an important feature, as the complexity of individualized homeopathic prescribing is an obstacle both to its reproducibility in independent trials and its broad clinical adoption.

The author is currently working on a manuscript detailing the guidelines of the supportive homeopathic measures. Additionally, he will be publishing 3 detailed case reports involving Psorinum therapy, which will give further insight into the homeopathic supportive approach. Execution of this protocol is therefore likely to be feasible for practitioners in the near future.

The primary limiting factor of this study is the lack of a control for the effects of the supportive homeopathic measures. Since supportive homeopathic medicines were extensively used, it is quite possible the outcomes were due in part (or in chief) to their influence.

A phase III trial comparing Psorinum 6X plus conventional and homeopathic supportive care to 1) conventional treatment and 2) Psorinum 6X plus conventional (but not homeopathic) supportive care in treatment of advanced pancreatic cancer is currently underway.

In this study, the women with the highest reported intakes of total vegetables at baseline measure had an overall lower risk of recurrence and a lower risk of developing a new primary breast cancer.

In this study, the women with the highest reported intakes of total vegetables at baseline measure had an overall lower risk of recurrence and a lower risk of developing a new primary breast cancer. This effect was most pronounced in women taking tamoxifen, and the effect was the greatest in tamoxifen users who consumed the highest quantity of cruciferous vegetables. Essentially, this study suggests that vegetable intakes above the average US intakes increase the likelihood of disease-free survival in women taking tamoxifen. This beneficial effect is amplified with cruciferous vegetable intake.

The postulated mechanisms underlying this observed relationship include the synergistic role of indole-3-carbinol (I3C) found in broccoli with tamoxifen in inducing apoptosis over tamoxifen alone. Additionally, diindolylmethane (DIM), a metabolic end-product of I3C influences the metabolism of tamoxifen away from tamoxifen N-oxide, a relatively inactive metabolite, and toward its active metabolite, 4-hydroxy tamoxifen. Other studies have demonstrated that sulfurophane, another component of broccoli, induces apoptosis in breast cancer stem cells,1 an action that theoretically would complement and strengthen the antiproliferative effects of tamoxifen.
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The findings in this secondary analysis are consistent with another recent study, which demonstrated that intake of 1 serving of raw broccoli, but not cooked broccoli or vegetables overall, at least once a month reduced the risk of dying from bladder cancer by 57% (HR for disease-specific death: 0.43; 95% CI: 0.25–0.74)2. This effect was attributed to isothiocyanates, which are destroyed in the cooking of broccoli.

The data from this secondary analysis is the latest addition to several studies elucidating the benefit of vegetable intake, and cruciferous vegetables in particular, on reducing the risk of cancer recurrence. The benefit of regular consumption of cruciferous vegetables, and broccoli in particular, on reducing the risk of breast cancer recurrence in tamoxifen users are worth notice. Tamoxifen has rapidly become part of standard care for women with estrogen receptor–positive breast cancer, which represents the majority of breast cancers. Thus, the inclusion of cruciferous vegetables in the daily diet of these women is important. The amount needed for this survival benefit is reasonable for most—a baseline of 0.5 servings per day—making this an acceptable strategy.

Limitations
This study was limited by the reliance upon self-reported data and thus the possibility of recall bias. Additionally, the data from this study cannot be generalized to other cohorts. Finally, as a secondary analysis, the conclusions should be verified in an independent study.

Design
Secondary analysis from the Women’s Healthy Eating and Living Study (WHEL study)

Participants
3,080 female breast cancer survivors aged 18–70, who were on average 23.5 months post-diagnosis at the time of enrollment. All participants lived in 4 western states, and the WHEL trial was conducted between the years of 1995 and 2006. Participants were diagnosed with and had completed treatment for stage I, II, or III invasive breast cancer, and at the time of enrollment were found to be without evidence of disease. The majority of participants were educated, nonsmoking, sedentary Caucasian women.

Study Parameters Assessed
The WHEL study intervention diet included a daily diet of 5 vegetables (a vegetable serving was defined as any ½-cup serving of raw or cooked vegetables or 1 cup of raw leafy vegetables excluding iceberg lettuce and white potatoes), 3 fruits, 16 oz. vegetable juice, 30 g fiber, and 20% energy from fat. The WHEL Study protocol included a baseline clinic visit to assess baseline characteristics. Dietary intakes were then assessed in 24-hour dietary recalls in 4 prescheduled telephone calls. At study entry (baseline), participants completed questionnaires regarding menopause history, use of menopausal hormone therapy, other lifestyle behaviors and cancer occurrence. Cancer outcomes were assessed from annual self-administered questionnaires, with 93% of cancers confirmed with a review of pathology reports.

In this secondary analysis, a separate subgroup analysis was performed on the effect of vegetable intake on recurrence in women taking tamoxifen compared to women not taking tamoxifen. Furthermore, the effect of cruciferous vegetable intake on recurrence rate in tamoxifen users was assessed.

Key Findings
WHEL participants reported mean baseline intakes of 3. 1 servings of total vegetables and 0.5 servings of cruciferous vegetables. Women in the highest tertile of vegetable intake had a significantly lower hazard of breast cancer recurrence (HR 0.69, 95% CI: 0.55–0.87) at baseline. Cruciferous vegetable intake did not produce a statistically significant decrease in the hazard of recurrence at baseline. This secondary analysis revealed that when stratified for tamoxifen use, hazard of recurrence was even lower in women in the highest tertile of vegetable intake versus non-tamoxifen users (HR 0.56, 95% CI: 0.41–0.77, P≤0.001). Furthermore, a statistically significant reduction in the hazard of recurrence was seen with cruciferous vegetable consumption in the tamoxifen users (HR 0.65, 95% CI: 0.47–0.89, P=0.006).

Practice Implications
This secondary analysis adds to the growing number of secondary analyses of the WHEL study that elucidate benefit from vegetable intake in subpopulations of the participants. Although the WHEL study ultimately failed to find benefit from consumption of vegetables in reducing the risk of breast cancer recurrence, subsequent secondary analyses of various cohorts, such as this one, are finding benefit.

Not all studies have found a protective role for aspirin in cancer development. The Nurses’ Health Study, which used 100 mg every other day, did not show any reduction in the incidence of cancer. The Physician’s Health Study failed to show any difference in colon cancer or adenoma development in those that who aspirin, although this study only spanned 7 years. According to the cited study above, this may not be enough time as there was a 10-year latency period for a reduction in deaths from colon cancer. It appears that if there is a benefit for aspirin usage in lessening incidence of cancer or cancer deaths, its use should be daily and at a low dose for an extended period of time (greater than 5 years). This implies that those in their 40s or 50s may derive more benefit from a longer duration of intake. As the authors point out, there is no evidence of what to expect beyond 20 years.

There is a sufficient body of evidence implicating inflammatory mediators, including cyclooxygenase-2, in the carcinogenic, tumorigenic, and metastatic processes. Looking at this study from a broader physiological perspective, the question it may also be asking is, “Does lowering inflammation through cox-2 inhibition affect cancer death rates?” Granted, it is possible that aspirin’s effects are from another mechanism, but given the established role of inflammation in carcinogenesis, aspirin’s cox-2 inhibition is the putative mechanism to date. This is important conceptually, as there are many other means of affecting inflammation, many without any risk to the patient. These include whole-food diets, select herbs, fish oil, stress reduction, and proper sleep. To what extent is aspirin’s effect on lowering inflammation a convenient substitute for more meaningful changes in diet and lifestyle? This is a rhetorical question, as the number of confounding factors affecting inflammation would be nearly impossible to account for in any study design.
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The widespread use of any drug should be considered with great caution.
While low-dose aspirin has some risk of gastric irritation and bleeding, the data in the above publication is compelling in that this risk appears minimal compared to the benefits for most people.
While low-dose aspirin has some risk of gastric irritation and bleeding, the data in the above publication is compelling in that this risk appears minimal compared to the benefits for most people. That said, each patient should be assessed for risk of bleeding—particularly gastrointestinal bleeds.

Study Limitations
This data was culled from studies that originally were assessing aspirin as a primary or secondary intervention for cardiovascular disease/events. The trials were not designed to assess aspirin’s effects on cancer incidence or mortality. In addition, the data is only as good as the source, and death certificates may or may not accurately represent cancer as the cause of death. For example, a patient with cancer may die due to complications from the disease or treatment (e.g., infection, stroke), and this complication may be documented as the cause of actual death. Prospective trials are needed to support the conclusions from the above study.

Since all of the longer-term (20-year) data was derived from U.K. databases only, there is some dietary bias that may not be applicable to other populaces. The authors concede that “the benefits of aspirin may be less in populations with a high dietary intake of salicylates.” Assessment of salicylate intake at baseline and throughout may be helpful in the future.