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Health Protocols

Breast Cancer

Integrative Interventions

Green Tea

Green tea and its components have been associated with numerous health benefits (Rafieian-Kopaei 2017). Consumption of green tea may improve outcomes after breast cancer diagnosis (Sinha 2017; Ogunleye 2010). About 500 Chinese women with triple-negative breast cancer were interviewed about their tea consumption. The risk of breast cancer recurrence was 46% lower among women who drank tea regularly during the five years after diagnosis than among those who did not drink tea. The vast majority of tea drinkers in this study drank green tea (Bao 2015). An earlier study found that consumption of at least three cups of green tea per day dramatically reduced the risk of recurrence of breast cancer, but only for women diagnosed with early-stage disease (Inoue 2001).

Data from these observational studies are encouraging, and randomized controlled trials are now testing whether adding green tea to the diet can improve survival. An exploratory dose escalation study found 600 mg of green tea extract twice daily was well-tolerated by women with a history of stage I-III breast cancer (Crew 2012). A subsequent study, using blood collected during the dose escalation study, found the extract reduced levels of hepatocyte growth factor and vascular endothelial growth factor, two proteins that play a role in tumor growth (Crew 2015).

Another study took a different approach. Women with early-stage breast cancer waiting for surgery took either green tea extract (2,175 mg containing about 940 mg EGCG per day, roughly equivalent to 8‒10 cups of green tea) or received no green tea for an average of 35 days prior to surgery. The women in the green tea extract group had reduced levels of proliferation markers in both benign and malignant cells from specimens obtained during surgery compared with the no tea group (Yu 2013).

Lastly, green tea may have additional benefits for breast cancer patients being treated with radiation therapy. In one study, women with breast cancer undergoing radiotherapy, and taking 400 mg capsules three times per day (total 1,200 mg) of EGCG for two to eight weeks, had several notable changes in growth factors and other growth-related markers in their blood. When serum from these patients was applied to human breast cancer cells in the lab, the cells stopped growing and began to die (Zhang, Wang 2012). Other studies have found that an EGCG-containing topical formula helps prevent progression of radiation-induced dermatitis when applied to the skin of breast cancer patients undergoing radiation therapy (Zhao 2016; Zhu 2016).


Flaxseed is a source of healthy fibers, omega-3 polyunsaturated fatty acids, and phytoestrogens called lignans (Kajla 2015). In laboratory studies, lignans have anti-cancer properties (Abarzua 2012; Mali 2017). In a Canadian observational study, eating flaxseed or flax bread at least weekly was associated with a reduced risk of breast cancer (Lowcock 2013).

Eating flaxseed may also be beneficial after breast cancer diagnosis (Mason 2014; Seibold 2014). One study followed over 1,000 women with breast cancer for several years. Postmenopausal women who ate the most lignans (at least 318 micrograms of lignans per day) were significantly more likely to have survived than those eating the least (less than 155 micrograms of lignans per day) (McCann 2010).

Lignans are converted in the gut to enterolignans, such as enterolactone (Patterson 2011). One study estimated enterolactone intake among 2,653 German postmenopausal women prior to breast cancer diagnosis who were followed about six years. Among those with the highest dietary enterolactone intake, the overall death rate was about 40% lower than among those with the lowest enterolactone intake (Buck 2011).

Smaller studies are beginning to address whether supplemental flaxseed can fight cancer. In a randomized clinical trial, women newly diagnosed with breast cancer ate either a flaxseed muffin (25 grams of flaxseed) or a placebo muffin daily for approximately one month before surgery. Levels of proliferation decreased and cell death increased in the tumors of those in the flax muffin group but not the control group (Thompson 2005). A second study evaluated secoisolariciresinol, a plant lignan that is converted to enterolactone in the gut. Among 45 women with benign breast hyperplasia, supplementation with 50 mg per day of secoisolariciresinol increased levels of enterolactone in the blood approximately nine-fold and decreased cellular proliferation in the affected breast tissue (Fabian 2010).


Selenium is an essential nutrient for humans. Brazil nuts are a particularly rich source of selenium. Other sources include some types of seafood (eg, tuna and crab), poultry, eggs, and wheat (Colpo 2013; Rayman 2000; Tinggi 2008). Comparing food history between 145 breast cancer cases and 148 control women in Iran suggested the women with a nutrient-rich diet, including selenium, may have a reduced risk of breast cancer (Vahid 2018). After breast cancer diagnosis, Polish women with low blood selenium (< 64.4 mcg/L) who were past smokers had higher mortality than women with the highest blood selenium (>81.0 mcg/L). An observational study using diet records showed Swedish women who smoked and had low estimated selenium intake before diagnosis may have reduced chances of survival (Lubinski 2017; Harris 2012). In one study, selenium levels were measured in the blood of 546 patients newly diagnosed with breast cancer. Women with the lowest levels of selenium were more than twice as likely to have died during the five-year follow up than women with the highest levels (Lubinski 2017). A second study found that breast cancer patients with high dietary intake of selenium were significantly less likely to die from the disease (Harris 2012).

Selenium may have interesting benefits for people with some BRCA1 mutations (Bera 2013). Proteins encoded by the BRCA genes are critical for repairing DNA and keeping the genome intact, and mutations in these genes lead to DNA damage and chromosome breaks. When people with BRCA1 mutations took 276 micrograms of supplemental selenium per day, in the form of sodium selenite, for one to three months, the frequency of chromosome breaks in their white blood cells was significantly reduced to the levels seen in non-carrier controls (Kowalska 2005). A second study found that selenium supplementation increased a marker of DNA repair in certain people with BRCA1 mutations (Dziaman 2009).

Se-methylselenocysteine (SeMSC) is a naturally occurring organic compound containing the mineral selenium. SeMSC is abundant in plants such as garlic, onions, and broccoli; it is a source of bioavailable selenium (Suzuki 2008; Lyi 2005). SeMSC has been shown to be an effective inhibitor of breast cell growth in laboratory studies and has significant anticancer activity (Sinha 1999; Sinha 1997). Moreover, in laboratory studies, SeMSC was a very effective selenium chemoprevention compound and caused cancer cells to self-destruct (Jung 2001; Suzuki 2010). In rats, exposure to SeMSC blocks the expansion of premalignant lesions at an early stage by simultaneously modulating pathways responsible for inhibiting cell proliferation and enhancing apoptosis (Ip 2001).

Different Forms of Selenium

The different forms of selenium have been shown to provide various protective properties against cancer, oxidative stress, DNA damage, and even shielding against toxic metal poisoning. For this reason, it is recommended to ingest a 200 microgram “cocktail” daily of various selenium forms to provide broad-spectrum coverage against the diseases of aging (Suzuki 2010; Lunoe 2011).

Here are brief descriptions of well-studied forms, highlighting how each can contribute to selenium-based protection against cancer.

  • Sodium selenite is a simple chemical salt of sodium and selenium. This form of selenium has the ability to ramp up our natural immune system to find and destroy tumor cells (Kiremidjian-Schumacher 2000; Asfour 2006).
  • Selenium-methyl L-selenocysteine triggers cancer cell suicide (apoptosis) and acts on more advanced cancer cells that have lost the fundamental “suicide gene” (Suzuki 2010).
  • Selenium from yeast provides advanced protection against oxidative stress and resulting DNA damage, to reduce the risks that a cell will undergo transformation into a malignancy (Richie 2014).

Because optimum cancer prevention requires protection from DNA damage, enhanced self-destruction of malignant cells, and a boosted immune system, the benefits of using multiple forms of selenium are obvious.

Omega-3 Polyunsaturated Fatty Acids

Long-chain omega-3 fatty acids—abundant in oily fish and flaxseed—are a type of lipid, which make up cell membranes. Greater omega-3 intakes may reduce the chance of breast cancer recurrence. In one trial, 3,081 women with early-stage breast cancer were monitored for about seven years. Women with the highest intakes of omega-3 fatty acids in their diets (at least 153 mg/day) were approximately 25% less likely to have a recurrence than women with the lowest intakes (Patterson, Flatt 2011). A second study followed 1,463 women for almost 15 years. Higher-than-average dietary intake of boiled or baked fish other than tuna (at least 3.85 grams per day) and the omega-3 fatty acid docosahexaenoic acid (DHA) (at least 60 mg per day) were associated with 34% and 27% reductions in risk of death, respectively, compared with those with minimal or no intake (Khankari 2015).

Some laboratory data suggest omega-3 fatty acids integrate into tumor cell membranes and make them more sensitive to chemotherapy (Fabian 2015; Vibet 2008). One phase II clinical trial treated women with metastatic breast cancer with 1.8 grams per day of DHA along with conventional chemotherapy. Although there was no control group in this trial, researchers found that women with the highest levels of DHA in their plasma membranes survived the longest (Bougnoux 2009).

Breast cancers have high numbers of inflammatory cells. The inflammation can contribute to tumor development and progression (Baumgarten 2012; Takeuchi 2017; Ben-Baruch 2003). Omega-3 fatty acids may help reduce inflammation (Fabian 2015). A 30-day randomized trial of 45 women with breast cancer compared markers of inflammation in women taking 1.8 grams per day of omega-3 fatty acids and a placebo group taking 2 grams per day of mineral oil. Levels of high sensitivity C-reactive protein, a marker of inflammation, increased in the placebo group during the course of the study but remained unchanged in the fatty acid group (Paixao 2017).

Omega-3 fatty acids may also help reduce certain side effects of conventional breast cancer treatment (Fabian 2015). Aromatase inhibitors can weaken bones, but a randomized placebo-controlled study on postmenopausal breast cancer survivors revealed that bone loss may be reduced if patients take 4 grams omega-3 fatty acids per day (Hutchins-Wiese 2014). Paclitaxel may cause peripheral neuropathy, or numbness in the hands and feet. In one study, breast cancer patients being treated with paclitaxel took either approximately 2 grams omega-3 fatty acids daily or placebo. The placebo group was twice as likely to experience peripheral neuropathy (Ghoreishi 2012). In addition to reducing the side effects of chemotherapy, omega-3 fatty acids in fish oil may also improve recovery from surgery in general (Heller 2004).


Various types of mushrooms have traditionally been used by several cultures to treat breast cancer. Modern research is beginning to validate and explore the benefits of these mushrooms for patients (Novaes 2011; Li 2014). In Japan, a component of the Coriolus versicolor mushroom, called polysaccharide K, has been used for decades as a cancer immunotherapy (Sun 2012). In China, several drugs based on Ganoderma sinense or C. versicolor have been approved (Jiang 2017; Chang, Zhang 2017).

Mainstream medicine in other parts of the world has been slower to study this therapeutic approach. In a recent analysis, extracts of the C. versicolor mushroom significantly improved chances of survival among patients with several types of cancer, including breast cancer (Eliza 2012).

Mushrooms may also help manage side effects of conventional treatment. Women taking extracts of Agaricus sylvaticus (2.1 grams per day) had better appetite and nutritional status than women taking a placebo (Valadares 2013). A powder form of Ganoderma lucidum (reishi mushroom) may reduce fatigue and improve quality of life for breast cancer patients (Zhao 2012).

Several studies have investigated the effects of various kinds of mushrooms on the immune system (Guggenheim 2014). The immune system is often suppressed in cancer patients, and some mushrooms may reverse this suppression and allow the immune system to fight the cancer again (Chang, Zhang 2017). G. lucidum was found to increase T cell numbers in cancer patients undergoing treatment (Jin 2012). An extract of Grifola frondosa (maitake) mushrooms (about 700 mg per day) increased the number and activity of natural killer (NK) cells and some types of T cells in breast cancer patients (Deng 2009). An extract of Trametes versicolor mushrooms (6 to 9 grams per day) (Torkelson 2012) or a combined extract of C. versicolor and Salvia miltiorrhiza (Wong 2005) had similar effects.


Melatonin, a hormone that regulates the sleep-wake cycle, is naturally produce by the body at night (Hill 2015; Brown 1994). For women with breast cancer, melatonin supplements may help them sleep while managing the symptoms of the disease itself or the side effects of treatment. For instance, women recovering from breast cancer surgery taking 6 mg melatonin about one hour before bedtime slept significantly better (Madsen 2016). In another study, the same dose of melatonin also reduced depression in a similar group of patients (Hansen 2014).

Disruption of sleep-wake cycles may increase the risk of breast cancer (Samuelsson 2017). For example, studies suggest night shift workers may be at increased risk (Viswanathan 2009; Hansen 2017). This effect may be partly due to reductions in melatonin levels in these workers. In laboratory studies, melatonin has demonstrated many anti-cancer properties (Reiter 2017). Supplemental melatonin slowed tumor growth in animal models (Hill 2015).

Data on supplemental melatonin in breast cancer patients are limited. One study enrolled 14 women with metastatic breast cancer who were not responding well to tamoxifen. The participants took 20 mg melatonin before bed. The cancer was stable in eight of the patients, and four patients responded (Lissoni, Barni 1995). The same research group conducted a follow-up randomized study in 40 patients with estrogen receptor-negative breast cancer. About half of the patients were treated with tamoxifen alone, and the others were treated with tamoxifen plus melatonin (20 mg/d). Seven of 19 patients treated with melatonin responded to treatment, but only two of 21 patients taking tamoxifen alone responded (Lissoni, Ardizzoia 1995).

Lastly, topical melatonin may help prevent skin irritation resulting from radiation therapy. In a phase II trial, melatonin or a placebo was applied to the skin of breast cancer patients during irradiation and two weeks after the end of the radiation therapy. Ninety percent of patients in the placebo group experienced mild or moderate radiation-induced skin irritation, but only 59% of the melatonin group were affected (Ben-David 2016).

Vitamin D

Vitamin D is synthesized in the skin during exposure to sunlight. In the winter, less than half of humans worldwide have the minimum recommended level of vitamin D in their blood (van Schoor 2017). Unfortunately, vitamin D levels may drop during treatment for breast cancer (Charehbili 2016).

Several studies suggest vitamin D is beneficial in women with breast cancer (Sofi 2017; Poole 2013; Hu 2017; Yao 2017). For instance, in a recent study that followed a group of women previously treated for breast cancer, those with high levels of vitamin D in their blood were 28% less likely to have died during the 8-year follow-up period than women with low levels (Yao 2017). A meta-analysis found that every 4 ng/mL increase in vitamin D level decreased the risk of breast cancer death by 6% (Hu 2017).

Data on vitamin D supplementation for women with breast cancer are limited. Several studies have found that supplementation with vitamin D can improve blood levels of vitamin D in patients taking the aromatase inhibitors letrozole or anastrozole (Arul Vijaya Vani 2016; Rastelli 2011; Khan 2010). Letrozole and other aromatase inhibitors may cause side effects in the bones or muscles. These symptoms are worse for women with low vitamin D levels, and supplementation may relieve these symptoms (Arul Vijaya Vani 2016; Khan 2010; Rastelli 2011; Khan 2017). One study found that 50,000 IU of vitamin D3 weekly added to daily standard-dose vitamin D and calcium supplementation reduced joint pain in women undergoing aromatase-inhibitor therapy. Importantly, only women whose 25-hydroxyvitamin D levels were 40 ng/mL or below received the 50,000 IU vitamin D supplementation, and there was no placebo control, only a control group treated with standard calcium plus vitamin D supplements. The beneficial effect was more pronounced in women with higher blood levels of 25-hydroxyvitamin D (more than 66 ng/mL) (Khan 2010).

Vitamin C

Vitamin C, or ascorbic acid, is abundant in fruits and vegetables. Vitamin C is important for immune health and protection of cells from free radicals (Carr 2017; Lobo 2010). Many cancer therapies are designed to destroy cancer cells with free radicals (Lopes 2017). Researchers have hypothesized that vitamin C may protect healthy cells from damage without protecting tumor cells (Greenlee 2009; Nechuta 2011; Greenlee 2012; Wintergerst 2006; Uetaki 2015). After diagnosis, breast cancer patients taking supplemental vitamins, including vitamin C, were 22% less likely to have a breast cancer recurrence after treatment than those not taking supplements (Nechuta 2011). A meta-analysis combining data on 17,696 women with breast cancer found that women taking vitamin C after diagnosis were 15% less likely to die from the disease than those not taking the supplement (Harris 2014).


Some studies found that breast cancer patients with low plasma levels of vitamin A precursors called carotenoids were more likely to have breast cancer recurrences after treatment (Eliassen 2015; Rock 2005). A pooled analysis of data from 18 prospective cohort studies found that several carotenoids were associated with reduced breast cancer risk. The protective carotenoids included alpha-carotene, beta-carotene, and beta-cryptoxanthin (Bae 2016). The best sources of carotenoids are a variety of fruits and vegetables, and in particular orange and yellow fruits and dark green, leafy vegetables (Maiani 2009).

Cruciferous Vegetables

Researchers encourage the inclusion of vegetables from the cruciferous family, such as broccoli, in the diet of women diagnosed with or at risk for breast cancer (Limon-Miro 2017). A meta-analysis confirmed that women with high amounts of cruciferous vegetables in their diet were less likely to be diagnosed with breast cancer (Liu 2013).

Cruciferous vegetables contain several beneficial compounds (Li 2017). In laboratory studies, a component called indole-3-carbinol (I3C) can slow the proliferation of tumor cells (Popolo 2017; Caruso 2014). I3C may induce favorable changes in the levels of different forms of estrogen, cause degradation of estrogen receptor alpha (the main receptor for estrogen), and reduce the activity of an enzyme that synthesizes estrogen (Marconett 2012; Licznerska 2013). In laboratory and animal models of hormone-dependent cancers, including breast cancer, I3C showed protection against tumor development (Popolo 2017; Tin 2014).

Diindolylmethane (DIM) is a byproduct of the metabolism of I3C (Thomson 2016). As with I3C, there is significant laboratory data suggesting that DIM has cancer-fighting properties. In mice, DIM inhibited breast cancer formation and reduced the growth of existing breast cancers (Thomson 2016; Chang 2005).  

The compound sulforaphane is also abundant in cruciferous vegetables. Sulforaphane is a potent inhibitor of breast cancer cells in laboratory studies (Pawlik 2013). There is growing evidence that sulforaphane’s effects are caused by changes to the DNA that affect the levels of proteins produced from certain genes (Atwell 2015; Gianfredi 2017). For instance, sulforaphane increased levels of the genes encoding two proteins that can slow tumor growth, phosphatase and tensin homolog (PTEN) and retinoic acid receptor-beta-2 (Gianfredi 2017; Lubecka-Pietruszewska 2015). Additionally, sulforaphane may enhance the effectiveness of the chemotherapy drugs 5-fluorouracil and paclitaxel against breast cancer cells (Milczarek 2017; Kim, Park 2017).

Studies of the anti-cancer effects of cruciferous vegetables and their molecular components in women with breast cancer or benign breast conditions are limited, but initial data are encouraging. A study assessed the dietary intake of cruciferous vegetables in 54 women with abnormal mammogram findings. Among women with DCIS, those with the highest levels of cruciferous vegetables in their diet had the lowest levels of a proliferation marker in their biopsy tissue samples (Zhang 2016).

In a randomized trial of women taking tamoxifen, supplementation with DIM (300 mg per day) improved several markers of estrogen metabolism (Thomson 2017). A study of postmenopausal women with early-stage breast cancer had similar beneficial results (Dalessandri 2004). Interestingly, DIM (300 mg per day) increased the expression of the BRCA1 gene among breast cancer patients with BRCA1 mutations (Kotsopoulos 2014). Lastly, in laboratory studies, DIM sensitized human breast cancer cells that were resistant to several drugs to radiation therapy (Wang, Lv 2016).

Milk Thistle

Silymarin, an extract of milk thistle, mainly consists of the lignan silybin (Bijak 2017). In laboratory studies, silymarin blocked proliferation of tumor cells, reduced inflammation, and protected cells from carcinogens (Agarwal 2006; Mahmoodi 2015).

Silybin may also improve the effects of chemotherapy. The chemotherapies paclitaxel and doxorubicin destroy breast cancer cells more effectively in the lab when cells are co-treated with silybin (Molavi 2017). One study in humans confirmed that a preparation of silybin effectively reached breast cancer tissues (Lazzeroni 2016), but the effect of silybin on breast cancer outcomes has not been tested.


Curcumin is a bright yellow component of the spice turmeric. In laboratory studies, curcumin can slow proliferation of breast cancer cells, cause tumor cells to die, and prevent tumors from developing blood vessels to supply nutrients (Wang, Yu 2016; Banik 2017; Khazaei Koohpar 2015). Curcumin may also specifically target cancer stem cells—rare tumor cells that can form new tumors (Mukherjee 2014; Charpentier 2014). Laboratory studies have also found that curcumin can make breast cancer cells more sensitive to chemotherapy drugs, including 5-fluorouracil, paclitaxel, and doxorubicin (Vinod 2013; Wang, Yu 2016; Sinha 2012; Panda 2017). A phase I clinical study using a combination of curcumin and docetaxel for patients with advanced and metastatic breast cancer found the combination to be well tolerated (Bayet-Robert 2010). Scientists looking into these anti-cancer effects of curcumin have found that curcumin alters many signaling pathways that cancer cells heavily rely on (Dandawate 2016).

Inflammation can promote tumor growth. In laboratory studies, curcumin can reduce the levels of inflammatory cytokines in breast cancer cells (Bachmeier 2008). One pro-inflammatory cytokine is tumor necrosis factor-alpha (TNF-α). In laboratory experiments, TNF-α changed the metabolism of tumor cells in a way that provided them with energy to sustain rapid growth. Treating the cells with curcumin blocked this effect of TNF-α (Vaughan 2013).

Curcumin may also help fight the way tumors protect themselves from the immune system (Wang, Yu 2016; Zhang 2007; Banik 2017). NK cells are often impaired in patients with cancer (Leischner 2016; Garner 1983). Mouse breast cancer cells treated with curcumin cannot suppress NK cells as effectively as untreated cells (Zhang 2007).

Tumors can also protect themselves using a type of suppressor T cell called a regulatory T cell or Treg. Treg cells dampen the immune response (Sakaguchi 2009; Ha 2009). When mice with breast cancer were treated with curcumin, the suppressive capacity of Treg cells was reduced and other T cells were able to destroy the tumor cells (Bhattacharyya 2010).


Apigenin, a flavone (ie, a class of flavonoids) present in fruits and vegetables (eg, onions, oranges, tea, celery, artichoke, parsley), has been shown to possess anti-inflammatory, antioxidant, and anti-cancer properties. Many studies have confirmed the cancer chemopreventive effects of apigenin (Sung 2016; Patel 2007).

Apigenin stimulates self-destruction or apoptosis in breast cancer cells (Tseng 2017; Chen 2007). One study showed that apigenin slowed the progression of human breast cancers in mice by inducing cell death, inhibiting cell proliferation, and reducing levels of HER2. Blood vessels responsible for feeding cancer cells were smaller in the apigenin-treated mice compared with untreated mice. Smaller vessels reduce the nutrient flow to the tumors and may deprive the cancer of nutrients (Mafuvadze 2012). Apigenin may also enhance the effects of the chemotherapy drugs paclitaxel and 5-fluorouracil (Seo 2017; Xu, Xin 2011; Choi 2009).

Blueberry Extract and Pterostilbene

Blueberries are rich in cancer-fighting compounds (Jeyabalan 2014). Mice with breast cancer fed a diet supplemented with blueberry extract powder had smaller tumors and fewer metastases than mice fed a control diet (Kanaya 2014). Most laboratory studies have tested the effects of one particular compound in blueberries, pterostilbene. Pterostilbene has been found to increase self-destruction (apoptosis) of breast cancer cells (Hung 2017), reduce proliferation of three subtypes of breast cancer (Wakimoto 2017), inhibit metastasis (Su 2015), and enhance the effects of tamoxifen (Mannal 2010).

Coenzyme Q10

Coenzyme Q10 (CoQ10) helps cellular enzymes turn food into energy. For several decades, it has been known that cancer patients often have decreased blood levels of CoQ10 (Lockwood 1994; Folkers 1996; Ren 1997). These findings sparked interest in the compound as a potential anti-cancer agent (NCCIH 2015).

In a clinical study, 32 patients were treated with CoQ10 (90 mg) in addition to other antioxidants and fatty acids; six of these patients showed partial tumor regression (Lockwood 1994). In one of these cases the dose of CoQ10 was increased to 390 mg and within one month the tumor was no longer palpable; after another month, mammography confirmed the absence of the tumor. A different patient with tumor tissue remaining after surgery took 300 mg of CoQ10, and within three months there was no residual tumor tissue. This complete regression of breast tumors in some patients, coupled with further reports of disappearance of breast cancer metastases (liver and elsewhere) in several other cases (Lockwood 1995) demonstrates the potential of CoQ10 as an adjuvant therapy for breast cancer. Although these promising data were reported more than 20 years ago, research on the effects of CoQ10 on breast cancer has been sparse since then (Tafazoli 2017).

Conjugated Linoleic Acid

Conjugated linoleic acid (CLA), found mostly in dairy and meat products, is a type of fat with some health-promoting properties (Chamruspollert 1999; Shokryzadan 2017). Some case-control studies suggest a diet rich in CLA can reduce the risk of breast cancer (Arab 2016). For instance, in one study, postmenopausal women with the highest CLA intake were 60% less likely to develop breast cancer compared with the group with the lowest intake (Aro 2000).

In one clinical trial, twenty-four women with stage I, II, or III breast cancer scheduled for surgery were treated with 7.5 grams of CLA per day (McGowan 2013). The authors found that a marker of cellular proliferation was decreased in the tumors after treatment compared with before treatment.


Pomegranate, which is rich in healthy polyphenols, has been used for centuries for medicinal purposes (Li 2017; Sharma 2017). Researchers discovered that treatment with whole pomegranate seed oil and juice concentrate resulted in dramatic growth inhibition of estrogen-dependent breast cancer cells in the lab (Kim 2002). The same study showed inhibition of tumor formation in rodent cells exposed to chemicals known to cause breast cancer. Using different methods, another research group found a 42% reduction in tumor formation in mice with pomegranate juice polyphenols and an 87% reduction with pomegranate seed oil (Mehta 2004).

Pomegranate seed oil is a potent inhibitor of aromatase, the enzyme that converts testosterone into estrogen (Adams 2010). This enzymatic blockade could contribute to the pomegranate seed oil’s ability to inhibit growth of estrogen-dependent breast cancer cells. Pomegranate extract has also been shown to enhance the effects of the estrogen-blocking drug tamoxifen (Banerjee 2011) and reduce levels of estrogen receptors in tumors (Mandal 2015). Pomegranate also increases apoptosis, even in cancer cells that lack estrogen receptors (Kim 2002).

Cancer cells need to grow new blood vessels to support their rapid growth and tissue invasion. They typically do this by ramping up production of certain growth factors, such as vascular endothelial growth factor (VEGF) (Kubota 2012). Pomegranate seed oil powerfully inhibits production of VEGF. In a laboratory model of vessel growth, these modulations translated into a significant decrease in new blood vessel formation (Toi 2003).

Pomegranate seed oil contains a number of unique chemical constituents with potent biological effects. Punicic acid, an omega-5 polyunsaturated fatty acid, inhibited both estrogen-dependent and estrogen-independent breast cancer cell proliferation in lab cultures and induced apoptosis at rates up to 91% higher than those in untreated cell cultures (Grossmann 2010).


Quercetin, a compound belonging to the group of pigments called flavonoids, is found in a broad range of plant foods, from grape skins and red onions to apples, green tea, and tomatoes. Quercetin can protect DNA from cancer-inducing mutations (Yasuda 2017). In breast cancer cells, quercetin stops tumor cells from dividing and causes them to self-destruct (Hashemzaei 2017; Balakrishnan 2017; Nguyen 2017). These effects inhibit the growth of tumors in mice (Hashemzaei 2017; Zhong 2003) and prolong survival of mice with breast cancer (Du 2010). Furthermore, quercetin favorably changes chemical signaling pathways that are abnormal in cancer cells (Morrow 2001; Bach 2010).

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the treatments discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. The publisher has not performed independent verification of the data contained herein, and expressly disclaim responsibility for any error in literature.