Breast Cancer

There are two types of tumours, they can be non-cancerous (benign) or cancerous (malignant). Breast cancerous tumours usually grow very slowly. It is shocking to note that scientists believe that by the time a tumour is large enough to be felt as a lump, it may have been growing for as long as 10 years already!

Frequently Asked Questions

  • 1What is breast cancer?
  • 2What are the symptoms of breast cancer?
  • 3What are the causes of breast cancer?
  • 4What are the risk factors for breast cancer?
  • 5What are additional causes of breast cancer?
  • 6What other factors influence breast cancer?
  • 7Why does conventional medicine sometimes fail in efforts to prevent breast cancer?
  • 8What are the risks and complications of this condition and its management?
  • 9How is breast cancer managed at Health Renewal?
  • 10What Natural supplements can be used to help treat/prevent cancer?
  • 11What diet is recommended?
  • 12Why should one not self-medicate?
  • 13How do I get started?
  • 14How often should I see the integrative Doctor?
  • 15How are genetic abnormalities passed on?
  • 16How is a non-genetic abnormality caused?
  • 17Why do some patients with a BRCA1 or BRCA2 mutation develop other forms of cancer at a relatively young age?
  • 18How does breast cancer develop in someone who as has acquired a BRCA1 or -2 mutation?
  • 19Why is genetic screening important?
  • 20Can a gene screening test be done for breast Cancer at Health Renewal?
  • 21Can a wellness gene test be done at Health Renewal?
  • 22How do we treat this at Health Renewal?
  • 23What should you bring along to your appointment with your Health Renewal doctor?
  • 24What is the cost of the extended consultation with the Health Renewal Doctor?
  • 25Health Renewal tip & Inspirational quotes for Healthy Living:

In a nutshell: Breast cancer occurs when cells in the breast tissue divide and grow without control. The cell cycle is the natural mechanism that regulates the growth and death of cells in the body. A failure of cell death (apoptosis) occurs when the normal cell regulators malfunction and cells do not die at the proper rate, this leads cell growth to go unchecked, allowing them to multiplying without any form of control. As a result, cancer begins to develop as cells divide without control, accumulating into a mass of extra tissue called a tumour. There are two types of tumours, they can be non-cancerous (benign) or cancerous (malignant). As a tumour grows, it elicits new blood vessel growth from the surrounding normal healthy tissues and diverts blood supply and nutrients away from this tissue to feed itself. This process is termed “angiogenesis” which refers to the development (genesis) of new blood vessels (angio). If there is unregulated tumour angiogenesis it facilitates the growth of cancer throughout the body, allowing the disease to spread and cause further havoc.

It is possible for cancer cells to leave the site of the original tumour, and to travel to distant locations, and recolonize. This process is called metastasis and it occurs commonly in organs such as the liver, lungs, and bones. Both the bloodstream and lymphatic system connect the entire body, which allows it to serve as an ideal vehicle for the traveling of cancer cells. The traveling cancer cells do not always survive beyond the tumour, but if they do survive, they will again begin to divide abnormally which will create tumours in each new location and spread the disease, making the situation worse. If a person leaves cancer untreated (or is not aware of it), or they have treatment-resistant cancer it will lead to eventually death due to the diseases. Once the vital organs, such as the liver or lungs are invaded, overtaken, and destroyed death is imminent.

Breast cancerous tumours usually grow very slowly. It is shocking to note that scientists believe that by the time a tumour is large enough to be felt as a lump, it may have been growing for as long as 10 years already! This has lead to the belief that undetectable spread of tumour cells (micrometastasis) may have already occurred by the time of the diagnosis. It is therefore imperative that woman take the necessary preventive measures such as maintaining a healthy balanced diet and lifestyle; to use nutritional supplementation, and to get enough exercise to protect them against the development of cancer. Early diagnosis is the best way to reduce the risk of dying from breast cancer. By making sure you perform a monthly self-breast exam, going for an annual clinical breast exam and screening mammography you can drastically improve your chances of early detection and subsequent treatment. If breast cancer is detected, there is no single treatment that will be enough as a cure. A multimodality approach will yield the best results, and this will include incorporating nutritional supplementation, making dietary modifications, detoxification, and one or more of the following: surgery, chemotherapy, radiation, hormone therapy, or vaccine therapy.

As explained above breast cancer begins in a single cell, which divides and multiplies at an uncontrolled rate. When the clump of cancer cells are in the beginning stages and still small, they are too tiny to be felt. This means that the earliest stages of breast cancer usually have no symptoms, or create a cause for worry. A mammogram is very effective in detecting cancer before you can feel a lump, which is why your annual screening mammogram is of vital importance. Some benign breast conditions can seem like cancer, so it’s good to know the difference, and get a health professional to check out worrisome lumps.

Signs and symptoms of breast cancer to look out for may include:

  • A breast lump or thickening that feels different from the surrounding tissue
  • Bloody discharge from the nipple
  • Change in the size or shape of a breast
  • Changes to the skin over the breast, such as dimpling
  • Inverted nipple
  • Peeling, scaling or flaking of the nipple or breast skin
  • Redness or pitting of the skin over your breast, which looks like the skin of an orange.

The cause of breast cancer is unclear. The only thing Doctors know is that breast cancer occurs when some breast cells begin growing abnormally. These cells divide more rapidly than healthy cells do and continue to accumulate, until it forms a visible/touchable lump or mass. The danger lies in when the cells may spread (metastasize) through the breast to the lymph nodes, from where it can move to other parts of the body. In most cases breast cancer begins with cells in the milk-producing ducts (invasive ductal carcinoma). Alternatively breast cancer may also begin in the glandular tissue called lobules (invasive lobular carcinoma) or in other cells within the breast. Researchers have identified specific things that can increase your risk of breast cancer, though nothing is set in stone. It is not clear why some people who have no risk factors develop cancer, yet other people with risk factors never do. It's likely that breast cancer is caused by a complex interaction of your genetic makeup and your environment.

Inherited breast cancer

Doctors estimate that only 5 to 10 per cent of breast cancers are linked to gene mutations passed through generations of a family. There are a number of inherited mutated genes that can increase the likelihood of breast cancer which have been identified. The two cancer genes’ that are most common (and that can lead to both breast & ovarian cancer) are breast cancer gene 1 (BRCA1) and breast cancer gene 2 (BRCA2). If you have a strong family history of breast cancer or other cancers, blood tests may help identify mutations in BRCA or other genes that are being passed through your family. Consider asking your doctor for a referral to a genetic counsellor, who can review your family health history. A genetic counsellor can also discuss the benefits, risks and limitations of genetic testing with you.

A wide variety of factors may influence an individual's likelihood of developing breast cancer; these factors are referred to as risk factors. Factors that are associated with an increased risk of breast cancer include:

  • Being female: Women are much more likely than men are to develop breast cancer.
  • Increasing age: Your risk of breast cancer increases as you age.
  • A personal history of breast cancer. If you've had breast cancer in one breast, you have an increased risk of developing cancer in the other breast.
  • A family history of breast cancer. If your mother, sister or daughter was diagnosed with breast cancer, particularly at a young age, your risk of breast cancer is increased. Still, the majority of people diagnosed with breast cancer have no family history of the disease.
  • Inherited genes that increase cancer risk. Certain gene mutations that increase the risk of breast cancer can be passed from parents to children. The most common gene mutations are referred to as BRCA1 and BRCA2. These genes can greatly increase your risk of breast cancer and other cancers, but they don't make cancer inevitable.
  • Radiation exposure. If you received radiation treatments to your chest as a child or young adult, your risk of breast cancer is increased.
  • Obesity: Being obese increases your risk of breast cancer.
  • Beginning your period at a younger age. Beginning your period before age 12 increases your risk of breast cancer.
  • Beginning menopause at an older age. If you began menopause at an older age, you're more likely to develop breast cancer.
  • Having your first child at an older age. Women who give birth to their first child after age 35 may have an increased risk of breast cancer.
  • Having never been pregnant. Women who have never been pregnant have a greater risk of breast cancer than do women who have had one or more pregnancies.
  • Postmenopausal hormone therapy. Women who take hormone therapy medications that combine estrogen and progesterone to treat the signs and symptoms of menopause have an increased risk of breast cancer. The risk of breast cancer decreases when women stop taking these medications.
  • Benign breast disease or breast trauma
  • Low physical activity,
  • Exposure to low-dose ionizing radiation in midlife and exposure to high-dose ionizing radiation early in life.
  • Having only one pregnancy rather than many
  • Not breast feeding after pregnancy,
  • A diet high in fat and low in fiber, fruits, and vegetables.

Alcohol is known to increase estrogen levels, which can have adverse effects. Studies have found that alcohol use appears to be more strongly associated with risk of lobular carcinomas and hormone receptor-positive tumours than it is with other types of breast cancer.


If a person partakes in exercising four or more hours a week it may decrease hormone levels and help lower breast cancer risk. The positive effect of exercise on breast cancer risk may be greatest in premenopausal women of normal or low weight. Regular exercise is an important part of being as healthy as you can be, and should be a goal for each individual. More and more research is showing that exercise can reduce the risk of breast cancer recurrence if you've been diagnosed, as well as reducing the risk of developing breast cancer if you’ve never been diagnosed.


A novel growth inhibitor recently identified as estrogen down-regulated gene 1 (EDG1) was found to be switched off (down-regulated) by estrogens. Inhibiting EDG1 expression in breast cells resulted in increased breast cell growth, whereas over-expression of EDG1 protein in breast cells resulted in decreased cell growth and decreased anchorage-independent growth, supporting the role of EDG1 in breast cancer.

Traditionally conventional medicine was aimed at treating the disease. In other words treatments were aimed at diagnosis and treatment of disease, and not so much on prevention. However this is changing and modern medical management strongly emphases preventative measures. “Prevention is better than cure”. Some of the treatments of breast cancer such as surgery, hormonal therapy, radiation and chemotherapy have side effects that can themselves cause suffering, illness and disease. The more aggressive treatments carry a high risk of adverse effects and so a patient deciding on treatment needs to be well informed. It is important to have more than one medical opinion before commencing on a treatment plan.

In the past 20 years, many strides have been made to improve the treatment of breast cancer. Some of the trauma associated with breast cancer treatment has been reduced because of increased early detection through mammography, surgery options that conserve much of the breast, and the increasing long-term survival rate. The treatment goal is to rid the body of the cancer as completely as possible and to prevent the cancer from returning. This is usually accomplished by utilizing multimodalities, including surgery, anticancer drugs (chemotherapy), irradiation, hormone therapy, nutritional supplementation, and diet modification.

Surgery and radiation therapy are considered local treatments. They focus on eliminating cancer from a limited or local area - such as the breast, chest wall, and axillary nodes. More systemic treatment options include chemotherapy, hormone therapy, nutritional supplementation, and diet modification. In systemic therapy, the entire body is treated in order to eradicate any cancer cells that may have spread from the breast tumour to other areas of the body.

Treatment depends on many factors, such as age, tumour stage, and estrogen-receptor status. However, deciding on a particular treatment is both a personal and a medical choice. Each treatment option has risks and benefits. Therefore, the type of treatment a woman chooses should be based on an understanding of how these risks and benefits relate to one's personal values and lifestyle.


There are two basic types of surgery for breast cancer: breast-conserving surgery or total mastectomy.

Breast-conserving surgery consists of the removal of the breast tumour and some of the surrounding normal tissue. This procedure can be referred to in various terms: a lumpectomy, wide excision, or partial-radical mastectomy. During the operation, axillary lymph nodes may also be removed.

A total mastectomy procedure is much more intense and entails the removal of the entire breast. As with breast conserving surgery, this may include an axillary dissection as well. For women who have decided to have breast reconstruction, this procedure will directly follow the mastectomy surgery or be performed at a later date.

All major surgery carries risks such as bleeding, swelling, lymphatic blockage, pain, slow healing, painful scarring, thrombosis and infection. However the risks of living with the cancer usually far outweigh the risks of surgery. With good post operation management risks are minimised, and the patient can continue life as normal

Radiation Therapy:

Radiation therapy (also known as radiotherapy) is considered a local treatment for breast cancer that uses targeted, high-energy x-rays to impede cancer cells' ability to grow and divide. Nearly all patients receiving radiation therapy will experience fatigue as a result of their treatment. Other side effects include breast heaviness and swelling from temporary lymphatic congestion. Irritation and redness of skin in the treated area or skin breakdown with peeling can occur. This skin reaction has similarities to a slowly developing sunburn. The redness and irritation will typically develop over a period of a few weeks. The patient's radiation oncology staff will discuss methods of treating these reactions, but in general, it is best to keep the affected skin clean and dry.


Chemotherapy uses drugs that can be taken in oral form or injected intravenously to kill cancer cells; sometimes, a combination of methods is used. While chemotherapy is an effective treatment for many women, it is associated with a number of well-known and traumatic side effects. These side effects can include hair loss, and exhausting bouts of nausea and vomiting, which many patients find difficult to tolerate. However, as research and technology advanced modern chemotherapy is generally well tolerated as there are medications to counteract and control the side effects.

Hormone Therapy:

Breast tumours often require hormones for growth, which poses a unique problem because the hormones involved in tumour growth are either estrogen, progesterone, or both. Hormone receptor-positive tumours can consist of cancer cells with receptor sites for estrogen, progesterone, or both. The hormones attach to receptor sites and promote cell proliferation. Hormone therapy blocks the hormones from attaching to the tumour receptor sites and may slow or stop the cancer's growth. The drug most often used in this type of endocrine therapy is tamoxifen. Other hormonal therapies are sometimes used, such as aromatase inhibitors (that inhibit the conversion of precursors to estrogens) or oophorectomy (the removal of the ovaries).

Tamoxifen has a host of side effects, including hot flashes, weight gain, mood swings, abnormal secretions from the vagina, fatigue, nausea, depression, loss of libido, headache, swelling of the limbs, decreased number of platelets, vaginal bleeding, blood clots in the large veins (deep venous thrombosis), blood clots in the lungs (pulmonary emboli), cataracts (Fisher et al. 1998), and the side effect of the greatest concern endometrial cancer (Harris et al. 1997).

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Natural Therapies:

Protecting Breast Cells against Dangerous Estrogens:

The stronger form of estrogen, estradiol, can be converted into the weaker form, estriol, in the body without using drugs. Estriol is considered to be a more desirable form of estrogen. It is less active than estradiol, so when it occupies the estrogen receptor, it blocks estradiol's strong "growth" signals. When using a natural substance the conversion of estradiol to estriol increased by 50% in 12 healthy people (Michnovicz et al. 1991). Furthermore, in female mice prone to developing breast cancer the natural substance reduced the incidence of cancer and the number of tumours significantly. The natural substance was indole-3-carbinol (I3C).

Indole-3-carbinol (I3C) is a phytochemical isolated from cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, turnips, kale, green cabbage, mustard seed, etc.). I3C given to 17 men and women for 2 months reduced the levels of strong estrogen, and increased the levels of weak estrogen. But more importantly, the level of an estrogen metabolite associated with breast and endometrial cancer, 16--a-hydroxyestrone, was reduced by I3C (Bradlow et al. 1991). When I3C changes "strong" estrogen to "weak" estrogen, the growth of human cancer cells is inhibited by 54-61% (Telang et al. 1997). Moreover, I3C provoked cancer cells to self-destruct (by killing themselves via apoptosis). Induction of cell death is an approach to suppress carcinogenesis and is the prime goal of cytotoxic chemotherapy. The increase in apoptosis induced by I3C before initiation of new tumor development may contribute to suppression of tumor progression. Nontoxic I3C can reliably facilitate apoptosis (12 week treatment in rats); thus, this phytonutrient may become a standard adjunct in the treatment of breast cancer (Zhang et al. 2003)

I3C inhibits human breast cancer cells (MCF7) from growing by as much as 90% in culture; growth arrest does not depend on estrogen receptors (Cover et al. 1998). Furthermore, I3C induces apoptosis in tumorigenic (cancerous) but not in nontumourigenic (non-cancerous) breast epithelial cells (Rahman et al. 2003). I3C does more than just turn strong estrogen to weak estrogen. 16-a-Hydroxyestrone (16-OHE) and 2-hydroxyestrone (2-OHE) are metabolites of estrogen in addition to estriol and estradiol. 2-OHE is biologically inactive, while 16-OHE is biologically active; that is, like estradiol, it can send "growth" signals. In breast cancer, the dangerous 16-OHE is often elevated, while the protective 2-OHE is decreased. Cancer-causing chemicals change the metabolism of estrogen so that 16-OHE is elevated. Studies show that people who take I3C have beneficial increases in the "weak" estriol form of estrogen and also increases in protective 2-OHE.

African-American women who consumed I3C, 400 mg for 5 days, experienced an increase in the "good" 2-OHE and a decrease of the "bad" 16-OHE. However, it was found that the minority of women who did not demonstrate an increase in 2-OHE, had a mutation in a gene that helps metabolize estrogen to the 2-OHE version. Those women had an eight times higher risk of breast cancer (Telang et al. 1997).


Tamoxifen is a drug prescribed to reduce breast cancer metastases and improve survival rates. I3C has modes of action that are similar to tamoxifen. I3C inhibited the growth of estrogen-receptor-positive breast cancer cells by 90% compared to 60% for tamoxifen. The mode of action attributed to I3C's impressive effect was interfering with the cancer cell growth cycle. Adding tamoxifen to I3C gave a 5% boost (95% total inhibition) (Cover et al. 1999).

In estrogen-receptor-negative cells, I3C stopped the synthesis of DNA by about 50%, whereas tamoxifen had no significant effect. I3C also restored p21 and other proteins that act as checkpoints during the synthesis of a new cell. Tamoxifen showed no effect on p21. Restoration of these growth regulators is extremely important. For example, tumour suppressor p53 works through p21 that I3C restores. I3C also inhibits cancers caused by chemicals. If animals are fed I3C before exposure to cancer-causing chemicals, DNA damage and cancer are virtually eliminated (Cover et al. 1999).

A study on rodents shows that damaged DNA in breast cells is reduced 91% by I3C. Similar results are seen in the liver (Devanaboyina et al. 1997). Female smokers taking 400 mg of I3C significantly reduced their levels of a major lung carcinogen. Cigarette chemicals are known to adversely affect estrogen metabolism (Taioli et al. 1997).

There is no proven way to prevent breast cancer, but the best and most comprehensive scientific evidence so far supports phytochemicals such as I3C (Meng et al. 2000). The results from a placebo-controlled, double-blind dose-ranging chemoprevention study on 60 women at increased risk for breast cancer demonstrated that I3C at a minimum effective dosage 300 mg per day is a promising agent for breast cancer prevention (Wong et al. 1997). The results of a single-blind phase I trial which studied the effectiveness of I3C in preventing breast cancer in non-smoking women who are at high risk of breast cancer are awaited. The rationale for this study is that I3C, ingested twice daily, may be effective at preventing breast cancer.

I3C was found to be superior to 80 other compounds, including tamoxifen, for anticancer potential. Indoles, which down-regulate estrogen receptors, have been proposed as promising agents in the treatment and prevention of cancer and autoimmune diseases such as multiple sclerosis, arthritis, and lupus. Replacement of all the chemically altered estrogen drugs, such as tamoxifen, with a new generation of chemically altered indole drugs that fit in the aryl-hydrocarbon (Ah) receptor and regulate estrogen indirectly may prove beneficial to cancer patients (Bitonti et al. 1999). An I3C tetrameric derivative (chemically derived) is currently a novel lead inhibitor of breast cancer cell growth, considered a new, promising therapeutic agent for both ER+ and ER- breast cancer (Brandi et al. 2003).

A summary of studies shows that indole-3-carbinol (I3C) can:

  • Increase the conversion of estradiol to the safer estriol by 50% in healthy people in just 1 week (Michnovicz et al. 1991)
  • Prevent the formation of the estrogen metabolite, 16,alpha-hydroxyestrone, that prompts breast cancer cells to grow (Chen et al. 1996), in both men and women in 2 months (Michnovicz et al. 1997)
  • Stop human cancer cells from growing (54-61%) and provoke the cells to self-destruct (apoptosis) (Telang et al. 1997)
  • Inhibit human breast cancer cells (MCF7) from growing by as much as 90% in vitro (Ricci et al. 1999)
  • Inhibit the growth of estrogen-receptor-positive breast cancer cells by 90%, compared to tamoxifen's 60%, by stopping the cell cycle (Cover et al. 1999)
  • Prevent chemically induced breast cancer in rodents by 70-96%. Prevent other types of cancer, including aflatoxin-induced liver cancer, leukemia, and colon cancer (Grubbs et al. 1995)
  • Inhibit free radicals, particularly those that cause the oxidation of fat (Shertzer et al. 1988)
  • Stop the synthesis of DNA by about 50% in estrogen-receptor-negative cells, whereas tamoxifen had no significant effect (Cover et al. 1998)
  • Restore p21 and other proteins that act as checkpoints during the synthesis of a new cancer cell. Tamoxifen has no effect on p21 (Cover et al. 1998)
  • Virtually eliminate DNA damage and cancer prior to exposure to cancer-causing chemicals (in animals fed I3C) (Grubbs et al. 1995)
  • Reduce DNA damage in breast cells by 91% (Devanaboyina et al. 1997)
  • Reduce levels of a major nitrosamine carcinogen in female smokers (Taioli et al. 1997)

How to Use I3C:

While the evidence is compelling, it is too soon to know exactly how effective I3C will be as an adjuvant breast cancer therapy.

Caution: Pregnant women should not take I3C because of its modulation of estrogen. I3C appears to act both at the ovarian and hypothalamic levels, whereas tamoxifen appears to act only on the hypothalamic-pituitary axis as an anti-estrogen. Both I3C and tamoxifen block ovulation by altering preovulatory concentrations of luteinizing hormone (LH) and follicle stimulating hormone (FSH) (Gao et al. 2002). The reported aversion to cruciferous vegetables by pregnant women may be associated with their ability to change estrogen metabolism. Estrogen is a necessary growth factor for the foetus.


Apigenin, which is a flavone (ie, a class of flavonoids) that is present in fruits and vegetables (eg, onions, oranges, tea, celery, artichoke, and parsley), has been shown to possess anti-inflammatory, antioxidant, and anticancer properties. Many studies have confirmed the cancer chemopreventive effects of apigenin (Patel 2007). Apigenin stimulates apoptosis in breast cancer cells (Chen 2007). A 2012 study showed that apigenin slowed the progression of human breast cancer by inducing cell death, inhibiting cell proliferation, and reducing expression of a gene associated with cancer growth (Her2/neu). In another study, it was noted that blood vessels responsible for feeding cancer cells were smaller in apigenin-treated mice compared to untreated mice. This is significant because smaller vessels mean restricted nutrient flow to the tumours and may have served to starve the cancer as well as limit its ability to spread (Mafuvadze 2012). Apigenin has been proven to have a synergistic treatment effect when combined with the chemotherapy drug paclitaxel (Xu 2011). In a study, apigenin increased the efficacy of the chemotherapy drug 5-Fluorouracil against breast cancer cells (Choi 2009).


Astragalus, an herb used for centuries in Asia, has exhibited immune-stimulatory effects. Astragalus potentiates lymphokine-activated killer cells (Chu 1988). One study found that astragalus could partially restore depressed immune function in tumor-bearing mice (Cho 2007a), while another concluded that “…astragalus could exhibit anti-tumor effects, which might be achieved through activating the…anti-tumor immune mechanism of the host” (Cho 2007b). It was observed in a clinical trial that astragalus inhibited the proliferation of breast cancer cells. Authors of the study stated, “The antiproliferation mechanisms may be related to its effects of up-regulating the expressions of p53…” (Ye 2011). Similar findings were noted in a previous experiment (Deng 2009).


Blueberries are rich in anthocyanins (ie, dark pigments in fruits) and pterostilbenes (ie, antioxidant closely related to resveratrol). The anti-cancer effects of blueberries are mediated by multiple mechanisms: Blueberry extracts block DNA damage. Damage to cellular DNA underlies most forms of cancer. By preventing such damage, blueberry extracts can block the malignant transformation of healthy cells (Aiyer 2008). Blueberry extracts inhibit angiogenesis. Rapidly-growing cancers recruit new blood vessels to meet their ravenous appetites for nutrients and oxygen. Blueberry inhibits new tumour blood vessel growth, known as angiogenesis (Gordillo 2009; Liu 2011). Blueberry extracts trigger cancer cells’ suicide. If normal cells replicate too fast, they are programmed to die through apoptosis. Cancerous cells, by contrast, ignore that programming, constantly doubling their population unchecked. Blueberry components restore normal programming and induce apoptosis in cells from a variety of cancers, putting the brakes on their rapid growth (Katsube 2003; Yi 2005; Seeram 2006; Srivastava 2007; Alosi 2010). Blueberry extracts stop excessive proliferation. Uncontrolled cell reproduction results in formation of dangerous tumours, as cells ignore the normal signals to stop growing. By restoring normal cellular signalling, blueberry extracts stop such out-of-control proliferation (Yi 2005; Adams 2010; Nguyen 2010). In an experimental breast cancer cell line, blueberry significantly reduced breast cancer cell proliferation, leading the researchers to state that “blueberry anthocyanins … demonstrated anticancer properties by inhibiting cancer cell proliferation and by acting as cell anti-invasive factors and chemo-inhibitors” (Faria 2010). In rats with experimentally induced breast cancer, the volume of new breast tumour formation was reduced by 40% in the group of rats supplemented with blueberry compared to the control group (Srinivasan 2008).

Blueberry extracts slow tumor spread by invasion and metastasis. Solid cancers produce matrix metalloproteinases, which are “protein-melting” enzymes that help them invade adjacent tissues and that enable them to metastasize. Blueberry extracts block matrix metalloproteinases, thereby inhibiting cancer invasion and metastasis (Adams 2010a; Matchett 2005). In one experiment published in 2011, blueberry extract was administered to mice with breast cancer. Compared to the control group, tumour volume was 75% lower in mice fed blueberry extract. Moreover, mice fed blueberry extract developed 70% fewer liver metastases and 25% fewer lymph node metastases compared to the control group (Adams 2011).


Breast cancers that are estrogen-receptor positive can grow and be exacerbated in the presence of estrogen in the body. One aim of drug therapy for estrogen-receptor positive breast cancer is to decrease the levels of estrogen in the body. To that end, drugs used to block the enzyme (ie, aromatase) that converts testosterone into estrogen (ie, aromatase inhibitors) are widely used in women with estrogen-receptor positive breast cancer. Chrysin, a flavonoid, is a natural aromatase inhibitor (Campbell 1993; Mohammed 2011).


Coffee, especially brews enriched with chlorogenic acid, protect cells against the DNA damage that leads to aging and cancer development (Bakuradze 2011; Hoelzl 2010; Misik 2010). Growing tumours develop the ability to invade local and regional tissue by increasing their production of “protein-melting” enzymes called matrix metalloproteinases. Chlorogenic acid—present in coffee—strongly inhibited matrix metalloproteinase activity (Jin 2005; Belkaid 2006). A 2011 study reported that postmenopausal women who drank 5 cups of coffee daily exhibited a 57% decreased risk of developing estrogen-receptor negative (non-hormone-responsive) breast cancer (Li 2011). Chlorogenic acid and other polyphenols are the likely beneficial agents in such cancers (Bageman 2008).


Curcumin is extracted from the spice turmeric and is responsible for the orange/yellow pigment that gives the spice its unique colour. Turmeric is a perennial herb of the ginger family and a major component of curry powder. Chinese and Indian people, both in herbal medicine and in food preparation, have safely used it for centuries. Curcumin has a number of biological effects in the body. However, one of the most important functions is curcumin's ability to inhibit growth signals emitted by tumour cells that elicit angiogenesis (growth and development of new blood vessels into the tumour). Curcumin inhibits the epidermal growth factor receptor and is up to 90% effective in a dose-dependent manner. It is important to note that while curcumin has been shown to be up to 90% effective in inhibiting the expression of the epidermal growth factor receptor on cancer cell membranes, this does not mean it will be effective in 90% of cancer patients or reduce tumour volume by 90%. However, because two-thirds of all cancers overexpress the epidermal growth factor receptor and such overexpression frequently fuels the metastatic spread of the cancer throughout the body, suppression of this receptor is desirable.

There are several other anticancer mechanisms of curcumin and based on the favourable results, higher-dose curcumin would appear to be useful for cancer patients to take. However, as far as curcumin being taken at the same time as chemotherapy drugs, there are contradictions in the scientific literature. Therefore, caution is advised. Please refer to the Cancer Chemotherapy protocol before considering combining curcumin with chemotherapy. Curcumin's effects are a dose dependent response, and a standardized product is essential. The recommended dose is four 900-mg capsules 3 times per day, preferably with food.

Green Tea

As a tumour grows it elicits new capillary growth (angiogenesis) from the surrounding normal tissues and diverts blood supply and nutrients away from the tissue to feed itself. Unregulated tumour angiogenesis can facilitate the growth of cancer throughout the body. Anti-angiogenesis agents, including green tea, inhibit this new tumour blood vessel (capillary) growth.

Green tea contains epigallocatechin gallate EGCG, a polyphenol that helps to block the induction of vascular endothelial growth factor (VEGF). Scientists consider VEGF essential in the process of angiogenesis and tumour endothelial cell survival. It is the EGCG fraction of green tea that makes it a potentially effective adjunct therapy in the treatment of breast cancer. In vivo studies have shown green tea extracts to have the following actions on human cancer cells (Jung et al. 2001b; Muraoka et al. 2002):

  • Inhibition of tumour growth by 58%
  • Inhibition of activation of nuclear factor-kappa beta
  • Inhibition of microvessel density by 30%
  • Inhibition of tumour-cell proliferation in vitro by 27%
  • Increased tumour-cell apoptosis 1.9-fold
  • Increased tumour endothelial-cell apoptosis threefold

The most current research shows that green tea may have a beneficial effect in treating cancer. While drinking green tea is a well-documented method of preventing cancer, it is difficult for the cancer patient to obtain a sufficient quantity of EGCG anticancer components in that form. Standardized green tea extract is more useful then green tea itself because the dose of EGCG can be precisely monitored and greater doses can be ingested without excessive intake of liquids. A suggested dose for a person with breast cancer is 5 capsules of 350-mg lightly caffeinated green tea extract 3 times a day with each meal. Each capsule should provide at least 100 mg of EGCG. It may be desirable to take a decaffeinated version of green tea extract in the evening to ensure that the caffeine does not interfere with sleep. Those patients that are sensitive to caffeine may also use this decaffeinated form for all treatment. However, there are benefits to obtaining some caffeine. Studies show that caffeine potentiates the anticancer effects of tea polyphenols, including the critical EGCG. Caffeine will be discussed in further detail later in this protocol. Green tea extract is available in a decaffeinated form for those sensitive to caffeine or those who want to take the less-stimulating decaffeinated green tea extract capsules for their evening dose.

Conjugated Linoleic Acid (CLA)

Conjugated linoleic acid (CLA) found naturally, as a component of beef and milk, refers to isomers of octadecadienoic acid with conjugated double bonds. CLA is essential for the transport of dietary fat into cells, where it is used to build muscle and produce energy. CLA is incorporated into the neutral lipids of mammary fat (adipocyte) cells, where it serves as a local reservoir of CLA. It has been proposed that CLA may be an excellent candidate for prevention of breast cancer (Ip et al. 2003). Low levels of CLA are found in breast cancer patients but these do not influence survival. Nevertheless, it has been hypothesized that a higher intake of CLA might have a protective effect on the risk of metastasis (Chajes et al. 2003).

CLA was shown to prevent mammary cancer in rats if given before the onset of puberty. CLA ingested during the time of the "promotion" phase of cancer development conferred substantial protection from further development of breast cancer in the rats by inducing cell kill of pre-cancerous lesions (Ip et al. 1999b). It was determined that feeding CLA to female rats while they were young and still developing conferred life-long protection against breast cancer. This preventative action was achieved by adding enough CLA to equal 0.8% of the animal's total diet (Ip et al. 1999a).

CLA inhibits the proliferation of human breast cancer cells (MCF-7), induced by estradiol and insulin (but not EGF). In fact, CLA caused cell kill (cytotoxicity) when tumour cells were induced with insulin (Chujo et al. 2003). The antiproliferative effects of CLA are partly due to their ability to elicit a p53 response that leads to growth arrest (Kemp et al. 2003). CLA elicits cell killing effects in human breast tumour cells through both p53-dependent and p53 independent pathways according to the cell type (Majumder et al. 2002). Refer to Cancer Treatment The Critical Factors, for more information on determining the p53 status of cancer. The effects of CLA are mediated by both direct action (on the epithelium) as well as indirect action through the stroma. The growth suppressing effect of CLA may be partly due to changes in arachidonic distribution among cellular lipids and an altered prostaglandin profile (Miller et al. 2001). Intracellular lipids may become more susceptible to oxidative stress to the point of producing a cytotoxic effect (Devery et al. 2001). CLA has the ability to suppress arachidonic acid. Since arachidonic acid can produce inflammatory compounds that can promote cancer proliferation, this may be yet another explanation for CLA's anticancer effects.

The recommended dose for CLA is a dose of 3000-4000 mg daily, which is approximately 1% of the average human diet. The suggested amount required to obtain the overall cancer-preventing effects is only 3000-4000 mg daily in divided doses.


Caffeine occurs naturally in green tea and has been shown to potentiate the anticancer effects of tea polyphenols. Caffeine is a model radio-sensitizing agent that is thought to work by abolishing the radiation-induced G2-phase checkpoint in the cell cycle. Caffeine can induce apoptosis of a human lung carcinoma cell line by itself and it can act synergistically with radiation to induce tumour cell kill and cell growth arrest. The cancer cell killing effect of caffeine is dependent on the dose (Qi et al. 2002).

Caffeine enhances the tumour cell killing effects of anticancer drugs and radiation. A preliminary report on radio-chemotherapy combined with caffeine for high-grade soft tissue sarcomas in 17 patients, (treated with cisplatin, caffeine, and doxorubicin after radiation therapy) determined complete response in six patients, partial response in six and no change in five patients. The effectiveness rate of caffeine-potentiated radio-chemotherapy was therefore 17%, and contributed to a satisfactory local response and the success of function-saving surgery for high-grade soft tissue sarcomas (Tsuchiya et al. 2000).

In a randomized, double blind placebo-controlled crossover study, the effects of caffeine as an adjuvant to morphine in advanced cancer patients was found to benefit the cognitive performance and reduce pain intensity (Mercadente et al. 2001). To ascertain the inhibitory effects of caffeine, mice at high risk of developing malignant and non-malignant tumours (SKH-1), received oral caffeine as their sole source of drinking fluid for 18-23 weeks. Results revealed that caffeine inhibited the formation and decreased the size of both non-malignant tumours and malignant tumours (Lou et al. 1999). Consumption of coffee, tea, and caffeine was not associated with breast cancer incidence in a study of 59,036 Swedish women (aged 40-76 years) (Michels et al. 2002).


Lignans are found in high concentrations in flaxseed and sesame. Once consumed, lignans are converted in the intestines into enterolactone.Enterolactone has been shown to inhibit angiogenesis and promote cancer cell apoptosis (Bergman 2007; Chen 2007). Enterolactone inhibits the aromatase enzyme, which converts testosterone into estrogen (Brooks 2005; Wang 1994). Researchers conducted an analysis of breast cancer risk and dietary lignan intake in 3158 women. They determined that premenopausal women with the highest lignan intake had a 44% reduced risk of developing breast cancer (McCann 2004).

Thirty-two women awaiting surgery for breast cancer were randomized to receive either a muffin containing 25 grams of flaxseeds or no flaxseed (control group). Post-operative analysis of the cancerous tissue revealed that markers of tumor growth were reduced by 30-71% in the flaxseed group versus no reduction in the control group (Thompson 2005). Scientists concluded that “dietary flaxseed has the potential to reduce tumor growth in patients with breast cancer.” In order to examine the relationship between dietary lignan intake and breast cancer, researchers assessed the diets of 1122 women in the 1-2 years before breast cancer diagnosis. They noted that postmenopausal women with the highest dietary intake of lignans had a 71% decreased risk of death from breast cancer (McCann 2010).


One of the most important supplements for a breast cancer patient is the hormone melatonin. Melatonin inhibits human breast cancer cell growth (Cos et al. 2000) and reduces tumour spread and invasiveness in vitro (Cos et al.1998). Indeed, it has been suggested that melatonin acts as a naturally occurring anti-estrogen on tumour cells, as it down-regulates hormones responsible for the growth of hormone-dependent mammary tumours (Torres-Farfan 2003). A high percentage of women with estrogen-receptor-positive breast cancer have low plasma melatonin levels (Brzezinski et al. 1997). There have been some studies demonstrating changes in melatonin levels in breast cancer patients; specifically, women with breast cancer were found to have lower melatonin levels than women without breast cancer (Oosthuizen et al. 1989). Normally, women undergo a seasonal variation in the production of certain hormones, such as melatonin. However, it was found that women with breast cancer did not have a seasonal variation in melatonin levels, as did the healthy women (Holdaway et al. 1997).

Low levels of melatonin have been associated with breast cancer occurrence and development. Women who work predominantly at night and are exposed to light, which inhibits melatonin production and alters the circadian rhythm, have an increased risk of breast cancer development (Schernhammer et al. 2003). In contrast, higher melatonin levels have been found in blind and visually impaired people, along with correspondingly lower incidences of cancer compared to those with normal vision, thus suggesting a role for melatonin in the reduction of cancer incidence (Feychting et al. 1998).

Light at night, regardless of duration or intensity, inhibits melatonin secretion and phase-shifts the circadian clock, possibly altering the cell growth rate that is regulated by the circadian rhythm (Travlos et al. 2001). Disruption of circadian rhythm is commonly observed among breast cancer patients (Mormont et al. 1997; Roenneberg et al. 2002) and contributes to cancer development and tumor progression. The circadian rhythm alone is a statistically significant predictor of survival time for breast cancer patients (Sephton et al. 2000).

Melatonin differs from the classic anti-estrogens such as tamoxifen in that it does not seem to bind to the estrogen receptor or interfere with the binding of estradiol to its receptor (Sanchez-Barcelo 2003). Melatonin does not cause side effects, such as those) caused by the conventional anti-estrogen drug tamoxifen. Furthermore, when melatonin and tamoxifen are combined, synergistic benefits occur. Moreover, melatonin can increase the therapeutic efficacy of tamoxifen (Lissoni et al.1995) and biological therapies such as IL-2 (Lissoni et al. 1994).

How melatonin interferes with estrogen signaling is unknown, though recent studies suggest that it acts through a cyclic adenosine monophosphate (cAMP)-independent signaling pathway (Torres-Farfan 2003). It has been proposed that melatonin suppresses the epidermal growth factor receptor (EGF-R) (Blask et al. 2002) and exerts its growth inhibitory effects by inducing differentiation (“normalizing” cancer cells)(Cos et al. 1996). Melatonin directly inhibits breast cancer cell proliferation (Ram et al. 2000) and boosts the production of immune components, including natural killer cells (NK cells) that have an ability to kill metastasized cancer cells.

In tumorigenesis studies, melatonin reduced the incidence and growth rate of breast tumors and slowed breast cancer development (Subramanian et al. 1991). Furthermore, prolonged oral melatonin administration significantly reduced the development of existing mammary tumors in animals (Rao et al. 2000). Melatonin can be safely taken for an indefinite period of time. The suggested dose of melatonin for breast cancer patients is 3-50 mg at bedtime. Initially, if melatonin is taken in large doses vivid dreams and morning drowsiness may occur. To avoid these minor side effects melatonin may be taken in low doses nightly and the dose slowly increased over a period of several weeks.


Pomegranate, which is rich in antioxidants, has gained widespread popularity as a functional food (i.e., for its health benefits). The health benefits of the fruit, juice(s), and extract(s) have been studied in relation to a variety of chornic diseases, including cancer (Syed 2012; Johanningsmeier 2011). Researchers discovered that consumption of whole pomegranate seed oil and juice concentrate (Kim 2002) resulted in dramatic growth inhibition of estrogen-dependent breast cancer cells. The same study showed inhibition of tumor formation in rodent cells exposed to known breast carcinogens. Using different methods, another research group found a 42% reduction in tumor formation with whole 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 contributes to 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, with the authors of a study stating that “…pomegranate combined with tamoxifen may represent a novel and a powerful approach to enhance and sensitize tamoxifen action” (Banerjee 2011). 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 (angiogenesis). They typically do this by ramping up production of a variety of growth factors, including VEGF and inflammatory interleukins. Pomegranate seed oil powerfully inhibits production of VEGF while upregulating production of migratory inhibitory factor (MIF) in breast cancer cells. In a laboratory model of vessel growth, these modulations translated into a significant decrease in new blood vessel formation (Toi 2003). Pomegranate seed oil’s capacity to block breast cancer development was also demonstrated in an organ culture model of mouse breast cancer (Mehta 2004).Treating the glands with pomegranate seed oil prior to exposure to a powerful carcinogen resulted in a 87% reduction in the number of cancerous lesions compared with controls.

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


PSK, which is a specially prepared polysaccharide extract from the mushroom Coriolus versicolor, has been studied extensively in Japan where it is used as a non-specific biological response modifier to enhance the immune system in cancer patients (Koda 2003; Noguchi 1995; Yokoe 1997). PSK suppresses tumor cell invasiveness by down-regulating several invasion-related factors (Zhang 2000). PSK has been shown to enhance NK cell activity in multiple studies (Ohwada 2006; Fisher 2002; Garcia-Lora 2001; Pedrinaci 1999). In a study investigating the use of PSK in women with stage 2 breast cancer, post-operative participants received Tamoxifen with PSK (3 g daily) or Tamoxifen alone. The 5-year survival was 89.9% in the PSK group compared to 86.9% in the group receiving Tamoxifen only (Morimoto 1996).


Pterostilbene, a polyphenol found in blueberries, grapes, and in the bark of the Indian Kino Tree, is closely related to resveratrol (but with unique attributes). Pterostilbene’s mechanisms of action include blocking enzymes that activate carcinogens (Mikstacka 2006, 2007), inducing apoptosis (Tolomeo 2005) and cell cycle arrest (Wang 2012), and enhancing nitric oxide-induced cell death (Ferrer 2007). Researchers observed that pterostilbene markedly inhibited the growth of breast cancer cells in the laboratory by inducing apoptosis and cell cycle arrest (Wang 2012).


Quercetin is a flavonoid found in a broad range of foods, from grape skins and red onions to green tea and tomatoes. Quercetin’s antioxidant and anti-inflammatory properties protect cellular DNA from cancer-inducing mutations (Aherne 1999). Quercetin traps developing cancer cells in the early phases of their replicative cycle, effectively preventing further malignant development and promoting cancer cell death (Yang 2006). Furthermore, quercetin favorably modulates chemical signaling pathways that are abnormal in cancer cells (Morrow 2001; Bach 2010). In breast cancer cells, quercetin induces apoptosis and cell cycle arrest (Choi 2001; Chou 2010). Querctin inhibited the growth of tumors (Zhong 2003) and prolonged survival of mice with breast cancer (Du 2010).


Se-methylselenocysteine (SeMSC), a naturally occurring organic selenium compound found to be an effective chemopreventive agent, is a new and better form of selenium. SeMSC is a selenoamino acid that is synthesized by plants such as garlic and broccoli. Methylselenocysteine (MSC) has been shown to be effective against mammary cell growth both in vivo and in vitro (Sinha et al. 1999) and has significant anticancer activity against mammary tumor development (Sinha et al. 1997). Moreover, Se-methylselenocysteine was one of the most effective selenium chemoprevention compounds and induced apoptosis in human leukemia cells (HL-60) in vitro (Jung et al. 2001a). Exposure to MSC blocks expansion of cancer colonies and premalignant lesions at an early stage by simultaneously modulating pathways responsible for inhibiting cell proliferation and enhancing apoptosis (Ip et al. 2000a).

Se-methylselenocysteine has been shown to:

  • Produce a 33% better reduction of cancerous lesions than selenite.
  • Produce a 50% decrease in tumor development.
  • Induce cell death (apoptosis) in cancer cells.
  • Inhibit cancer-cell growth (proliferation).
  • Reduce density and development of tumor blood vessels.
  • Down-regulate VEGF (vascular endothelial growth factor). (Ip et al. 1992; Sinha et al. 1997; Sinha et al. 1999; Ip et al. 2000a, b; Dong et al. 2001)

Unlike MSC, which is incorporated into protein in place of methionine, SeMSC is not incorporated into any protein, thereby offering a completely bioavailable compound. In animal studies, SeMSC has been shown to be 10 times less toxic than any other known form of selenium. Breast cancer patients may consider taking 400 mcg of SeSMC daily.


Sulforaphane, which is an isothiocyanate, is most highly concentrated in broccoli as well as in other cruciferous vegetables (eg, brussels sprouts, cabbage and cauliflower). Sulforaphane detoxifies potential carcinogens, promotes apoptosis, blocks the cell cycle that is required for cancer cell replication, prevents tumor invasion into healthy tissue, enhances natural killer cell activity, and combats metastasis (Zhang 2007; Nian 2009; Traka 2008; Thejass 2006). Research has also demonstrated that sulforaphane is among the plant chemicals most potently capable of blocking the cancer-producing effects of ultraviolet radiation (Dinkova-Kostova 2008).

It has been observed that sulforaphane activated apoptosis (Pledgie-Tracy 2007) and inhibited the proliferation of breast cancer cells in culture (Ramirez 2009; Jo 2007). The binding of estrogen hormones to estrogen receptor alphapromotesbreast cell proliferation, which can promote the progression of breast cancer. Researchers have also noted that sulforaphane down-regulates the expression of estrogen receptor alpha in breast cancer cells (Ramirez 2009). In another clinical trial, mice injected with breast cancer cells developed 60% less tumor mass when treated with sulforaphane compared to untreated mice (Jackson 2004).


Coenzyme Q10 (CoQ10) is synthesized in humans from tyrosine through a cascade of eight aromatic precursors. These precursors require eight vitamins, which are vitamin C, B2, B3 (niacin) B6, B12, folic acid, pantothenic acid, and tetrahydrobiopterin as their coenzymes. Since the 1960s, studies have shown that cancer patients often have decreased blood levels of coenzyme Q10 (Lockwood et al. 1995; Folkers 1996; Ren et al. 1997). In particular, breast cancer patients (with infiltrative ductal carcinoma) who underwent radical mastectomy were found to have significantly decreased tumour concentrations of CoQ10 compared to levels in normal surrounding tissues. Increased levels of reactive oxygen species may be involved in the consumption of CoQ10 (Portakal et al. 2000). These findings sparked interest in the compound as a potential anticancer agent (NCCAM 2002). Cellular and animal studies have found evidence that CoQ10 stimulates the immune system and can increase resistance to illness (Bliznakov et al. 1970; Hogenauer et al. 1981; NCCAM 2002). CoQ10 may induce protective effect on breast tissue and has demonstrated promise in treating breast cancer. Although there are only a few studies, the safe nature of CoQ10 coupled with this promising research of its bioenergetic activity suggests that breast cancer patients should take 100 mg up to 3 times a day. It is important to take CoQ10 with some kind of oil, such as fish or flax, because dry powder CoQ10 is not readily absorbed.

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. In one of these cases the dose of CoQ10 was increased to 390 mg and within one month the tumor was no longer palpable, within two months the mammography confirmed the absence of tumor. In another case, the patient took 300 mg of CoQ10 for residual tumor (post non-radical surgery) and within 3 months there was non residual tumor tissue (Lockwood et al. 1994). This overt complete regression of breast tumors in the latter two cases coupled with further reports of disappearance of breast cancer metastases (liver and elsewhere) in several other case (Lockwood et al. 1995) demonstrates the potential of CoQ10 in the adjuvant therapy of breast cancer. There are promising results for the use of CoQ10 in protecting against heart damage related to chemotherapy. Many chemotherapy drugs can cause damage to the heart (UTH 1998; ACS 2000; NCCAM 2000; Dog et al. 2001), and initial animal studies found that CoQ10 could reduce the adverse cardiac effects of these drugs (Combs et al. 1977; Choe et al. 1979; Lubawy et al. 1980; Usui et al. 1982; Shinozawa et al. 1993; Folkers 1996).

Caution: Some studies indicate that CoQ10 should not be taken at the same time as chemotherapy. If this were true, it would be disappointing, because CoQ10 is so effective in protecting against adriamycin-induced cardiomyopathy. Adriamycin is a chemotherapy drug sometimes used as part of a chemotherapy cocktail. Until more research is known, it is not possible to make a definitive recommendation concerning taking CoQ10 during chemotherapy. For more information please see the Cancer Chemotherapy protocol.


Dietary polyunsaturated fatty acids (PUFAs) of the omega-6 (n-6) class, found in corn oil and safflower oil, may be involved in the development of breast cancer, whereas long chain (LC) omega-3 (n-3) PUFAs, found in fish oil can inhibit breast cancer (Bagga et al. 2002). A case control study examining levels of fatty acids in breast adipose tissue of breast cancer patients has shown that total omega-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that omega-3 PUFAs, derived from fish oil, may have a protective effect (Bagga et al. 2002). A higher omega-3:omega-6 ratio ((n-3)):(n-6) ratio) may reduce the risk of breast cancer, especially in premenopausal women (Goodstine et al. 2003). In a prospective study of 35,298 Singapore Chinese women aged 45-74 years, it was determined that high levels of dietary omega-3 fatty acids from marine sources (fish/shellfish) were significantly associated with reduced risk of breast cancer. Furthermore, women who consumed low levels of marine omega-3 fatty acids had a statistically significant increased risk of breast cancer (Gago-Dominguez et al. 2003). Omega-3 fatty acids, primarily eicosapentanoic acid (EPA) and docosahexaneoic acid (DHA) found naturally in oily fish and fish oil, have been consistently shown to retard the growth of breast cancer in vitro and in animal experiments, inhibit tumor development and metastasis. Fish oils have antiproliferative effects at high doses, which means they can inhibit tumour cell growth, through a free radical-mediated mechanism, while at more moderate doses omega-3 fatty acids inhibit, Ras protein activity, angiogenesis, and inflammation. The production of pro-inflammatory cytokines can be modified by dietary omega-3 PUFAs (Mancuso et al. 1997).

High consumption of fatty fish is weakly associated with reduced breast cancer risk (Goodstine et al. 2003). Flaxseed, the richest source of alpha-linoleic acid inhibited the established growth and metastasis of human breast cancer implanted in mice. This effect was found to be due to its down-regulation of insulin-like growth factor I (IGF-1) and epidermal growth factor receptor (EGF-R) expression (Chen et al. 2002). The recommended dosage is to consume a fish-oil concentrate supplement that provides 3200 mg of EPA and 2400 mg of DHA a day taken in divided doses.

Vitamins A, D, and E

Vitamin A and vitamin D3 inhibit breast cancer cell division and can induce cancer cells to differentiate into mature, noncancerous cells. Vitamin D3 works synergistically with tamoxifen (and melatonin) to inhibit breast cancer cell proliferation. The vitamin D3 receptor as a target for breast cancer prevention was examined. Pre-clinical studies demonstrated that vitamin D compounds could reduce breast cancer development in animals. Furthermore, human studies indicate that both vitamin D status and genetic variations in the vitamin D3 receptor (VDR) may affect breast cancer risk. Findings from cellular, molecular and population studies suggest that the VDR is a nutritionally modulated growth-regulatory gene that may represent a molecular target for chemoprevention of breast cancer (Welsh et al. 2003). Daily doses of vitamin A, 350,000 to 500,000 IU were given to 100 patients with metastatic breast carcinoma treated by chemotherapy. A significant increase in the complete response was observed; however, response rates, duration of response and projected survival were only significantly increased in postmenopausal women with breast cancer (Israel et al. 1985).

Breast cancer patients may take between 4000 to 6000 IU, of vitamin D3 every day. Water-soluble vitamin A can be taken in doses of 100,000-300,000 IU every day. Monthly blood tests are needed to make sure toxicity does not occur in response to these high daily doses of vitamin A and vitamin D3. After 4-6 months, the doses of vitamin D3 and vitamin A can be reduced. Vitamin E is the term used to describe eight naturally occurring essential fat-soluble nutrients: alpha-, beta-, delta-, and gamma-tocopherols plus a class of compounds related to vitamin E called alpha-, beta-, delta-, and gamma-tocotrienols. Vitamin E from dietary sources may provide women with modest protection from breast cancer.

Vitamin E succinate, a derivative of fat-soluble vitamin E, has been shown to inhibit tumor cell growth in vitro and in vivo (Turley et al. 1997; Cameron et al. 2003). In estrogen receptor-negative human breast cancer cell lines vitamin E succinate inhibited growth and induced cell death. Since vitamin E is considered the main chain breaking lipophilic antioxidant in plasma and tissue, its role as a potential chemopreventative agent and its use in the adjuvant treatment of aggressive human breast cancers appears reasonable. Those with estrogen-receptor-negative breast cancers should consider taking 800-1200 IU of vitamin E succinate a day. Vitamin E supplementation, 800 IU daily for 4 weeks, was shown to significantly reduce hot flashes in breast cancer survivors (Barton et al. 1998).

Caution: it is possible to get Vitamin A Toxicity. When taking doses of vitamin D3 in excess of 1400 IU a day, regular blood chemistry tests should be taken to monitor kidney function and serum calcium metabolism. Vitamin E has potential blood thinning properties, individuals taking anticoagulant drugs should inform their treating physician if supplementing with vitamin E and have their clotting factors monitored regularly.


When vitamin E was isolated from plant oils, the term tocopherols was used to name the initial four compounds that shared similar structures. Their structures have two primary parts--a complex ring and a phytyl (long-saturated) side chain--and have been designated as alpha, beta, delta, and gamma tocopherol. Tocopherols (vitamin E) are important lipid-soluble antioxidants that can protect the body against free radical damage. However, there are four additional compounds related to tocopherols--called tocotrienols that are less widely distributed in nature. The tocotrienol structure, three double bonds in an isoprenoid (unsaturated) side chain, differs from that of tocopherols. While tocopherols are found in corn, olive oil, and soybeans, tocotrienols are concentrated in palm, rice bran, and barley oils.

Tocotrienols elicit powerful anticancer properties, and studies have confirmed tocotrienol activity is much stronger than that of tocopherols (Schwenke et al. 2002). Tocotrienols provide more efficient penetration into tissues such as the brain and liver. Because of the double bonds in the isoprenoid side chain, tocotrienols move freely and more efficiently within cell membranes than tocopherols, giving tocotrienols greater ability to counteract free radicals. This greater mobility also allows tocotrienols to recycle more quickly than alpha-tocopherol. Tocotrienols are better distributed in fatty cell membranes and demonstrate greater antioxidant and free-radical-scavenging effects than that of vitamin E (alpha-tocopherol) (Serbinova et al. 1991; Theriault et al. 1999). Tocotrienol's antioxidant function is associated with lowering DNA damage, tumour formation, and of cell damage. Animals exposed to carcinogens that were fed corn oil- or soybean oil-based diets had significantly more tumours than those fed a tocotrienol-rich palm oil diet. Tocotrienol-rich palm oil did not promote chemically induced breast cancer (Sundram et al. 1989). Tocotrienols possess the ability to stimulate the selective killing of cancer cells through programmed cell death (apoptosis) and to reduce cancer cell proliferation while leaving normal cells unaffected. Tocotrienols cause growth inhibition of breast cancer cells in culture independent of estrogen sensitivity and have great potential in the prevention and treatment of breast cancer (Nesaretnam et al. 1998). tamoxifen and tocotrienols may reduce the risk of adverse side effect from tamoxifen (Guthrie et al. 1997). Tocotrienols are considered important lipid-soluble antioxidants, with potent anticancer and anti-inflammatory activity. Therefore, a daily dose of 240 mg of tocotrienols should be considered as an adjuvant breast cancer therapy.

Cancer has an appetite for sugar and requires sugar for survival. Sugar plays an active role in reducing the immune response and energizes cancer, as tumours are primarily obligate glucose metabolizers.

There is a relationship between lactic acid, insulin, and angiogenesis. In tumours, hypoxic conditions occur through both inflammation, which reduces blood flow, and the chaotic development of blood vessels within tumours. These hypoxic conditions alter the pathways by which immune cells and tumor cells burn fuel (glucose) for energy, creating excessive lactic acid. In an oxygen-rich (aerobic) environment, glucose is burned in an efficient process that produces a maximum amount of energy and a minimal amount of lactic acid. However, tumour cells in chronic hypoxic conditions produce excessive lactic acid and inefficient utilization of glucose. Thus, there is a vicious cycle in which the reduced energy output stimulates the tumour cells to burn more glucose, which in turn produces more lactic acid. Tumour cells consume glucose at a rate three to five times higher than normal cells, creating a highly stimulated glycolysis (glucose-burning) pathway.

This glucose consumption can waste the cancer patient's energy reserves, and the increased production of lactic acid can stimulate increased production of angiogenic factors. The macrophage-mediated angiogenesis creates a complex interplay between opposing regulators. Insulin plays an active roll in promoting angiogenesis. Insulin is a growth factor that stimulates glycolysis and the proliferation of many cancer-cell lines through tyrosine kinase growth factors (Boyd 2003). In cancer patients, elevated levels of insulin are common in cancerous tissue and blood plasma. Obesity, and early stages of Type-II noninsulin-dependent diabetes mellitus (NIDDM), has been implicated as risk factors in a variety of cancers.

Based upon cancer's sugar dependency, a sugar-deprivation diet is strongly recommended. An effective tool in eliminating sugar from the diet is through following the Glycaemic Index. The index is a list that rates the speed at which foods are digested and raise blood sugar levels. The ratings are based upon the rate at which a measured amount of pure glucose affects the body's blood sugar curve. Glucose itself has a rating of 100, and the closer a food item is to a rating of 100, the more rapidly it raises blood glucose levels. Foods with a low Glycaemic Index, such as vegetables, protein, and grains, are suggested (please refer to the Obesity protocol for specific information about low glycemic foods).

It is vital to start depleting sugar from the diet, thus the following guidelines should be considered:

  • Limit or avoid all white (refined) foods, including (but not limited to) sugar, flour, rice, pasta, breads, crackers, cookies, etc.
  • Read ingredient labels carefully. Sugar has many names (brown sugar, corn syrup, honey, molasses, maple syrup, high-fructose corn syrup, dextrin, raw sugar, fructose, polyols, dextrose, hydrogenated starch, galactose, glucose, sorbitol, fruit juice concentrate, lactose, brown rice syrup, xylitol, sucrose, mannitol, sorghum, maltose, and turbinado, to mention only a few).
  • Limit all fruit juices; per glass they contain the juice of many pieces of fruit and a large amount of fructose (fruit sugar) but no fibre. Instead, infrequently eat low glycaemic-rated fruit in small portions.

Natural compounds have also been reported to inhibit the cancer-promoting effects of insulin. For example, vitamin C has been reported to increase oxygen consumption and reduce lactic acid production in tumor cells. In addition, some natural compounds may help reduce insulin production by reducing insulin resistance. Insulin resistance occurs when cells are no longer sensitive to insulin and thus more insulin is produced in an effort to reduce glucose levels. Insulin resistance has been implicated as a risk factor for breast cancer, and diets high in saturated fats and omega-6 fatty acids promote insulin resistance. Although the exact pathway is unknown, it is thought that the mechanism of action is via chronic activation of PKC. Some of the known natural compounds that can reduce insulin resistance include omega-3 fatty acids, curcumin, flavonoids, selenium, and vitamin E.

As discussed earlier in this section, estrogen is a growth factor for most breast cancers. High-fat diets and associated increases in fat tissue can increase estrogen availability in a number of ways:

  • Fat tissue is a major source of estrogen production in postmenopausal women. Therefore, there is an association between high body weight and decreased survival in breast cancer patients.
  • Obesity and possibly insulin resistance can decrease the levels of sex hormone binding globulin (SHBG) in both men and women and increase breast cancer risk or cancer progression. This is an important factor in estrogen-dependent breast cancer cells because it is adequate levels of SHBG that act as an anti-proliferative and provides an anti-estrogenic effect.
  • Obesity can alter liver metabolism of estrogen, allowing the retention of high estrogen byproducts with high estrogenic activity within the body.
  • High-fat diets may reduce the amount of estrogen excreted in the faeces. In contrast, low-fat/high-fibre diets can reduce circulating estrogen.

Another consideration when discussing diet and breast cancer is the reduction of dietary estrogen. Several foods contain naturally occurring hormones (found in animal sources); synthetic hormones that can mimic estrogen in the human body (found in commercially packaged meat, poultry, and dairy products); or naturally estrogenic properties that can encourage the body's production of estrogens (natural foods such as soy). Regardless of the source, try to avoid all commercial animal products (including, but not limited to, meats, poultry, and dairy). Also avoid the use of soft plastic food-storage products that can give off large amounts of polymers (e.g., by leaching into food contents), thought by environmentalists and some researchers to be a possible cause of breast cancer. In order to reduce estrogen, a breast cancer patient should consider increasing dietary intake of fish high in omega-3 fatty acids, whey, eggs, and nuts, occasionally including hormone-free poultry and hormone-free, low-fat dairy products.

When considering breast cancer treatment options, physicians and patients alike must sort through an overwhelming amount of information. This webpage attempts to simplify complicated scientific research and bring to the forefront the most up-to-date, multi-modality approach to cancer treatment. It integrates surgery, anticancer drugs, irradiation, hormone therapy, nutritional supplementation, and diet modification in a comprehensive approach to counteract breast cancer. What we do know is that there is overwhelming research supporting an integrated approach to the treatment of cancer. Additionally, research supports using nutritional supplementation to improve the efficacy of chemotherapy drugs and radiotherapy. In fact, combining certain supplements can create a synergism that can effectively block or impede certain cancer pathways.

But it is simply not possible for someone to objectively decide on what treatment to choose. Not all breast cancers are the same and therapy will be individualised and based on the type and stage of cancer. And so, it is imperative that any patient who is affected by breast cancer is managed by a breast cancer specialist, be that an oncologist or a breast surgeon or a radiation oncologist. The additional input from a doctor qualified in Integrative Medicine will assist with choosing the correct nutraceuticals and supplements that will augment the active treatments. It is essential to consult your physician before beginning any nutritional supplementation regimen.

Make an appointment to consult with your Health Renewal Doctor and he/she will assist you in determining your risk factors and how best to prevent any problems/ conditions that you may be susceptible to.

Blood tests may be taken and could include complete blood chemistry, with tests for liver function and serum calcium levels, prolactin, parathyroid hormone, and the tumour marker CA 27.29 (or CA 15.3). Additional blood tests to consider are the CEA and GGTP tests. These tests monitor the progress of therapies used and also detect toxicity from high doses of vitamin A and vitamin D3. The patient should insist on obtaining a copy of their blood workups every month.

Depending on which form of supplementation you and your Health Renewal Doctor have decided on, one could expect to follow up with your physician from anything between every 3 months to once every 6 months.

An inherited genetic abnormality can be passed on from a parent to a child (male or female), who has a 50% chance of inheriting the faulty gene (and a 50% chance of inheriting the normal copy of the gene).

An acquired (or non-hereditary) genetic abnormality is caused by an error during gene reproduction or from interaction with environmental factors such as hormonal influences, toxic exposure or by an inappropriate diet. Acquired genetic abnormalities account for more than 80% of breast cancers. Mutations in the BRCA1 and BRCA2 genes are the best-known cause of inherited breast cancer, but explain less than 5% of the total breast cancer incidence and approximately 20% of cases with a family history of breast cancer. A large proportion of familial breast cancer is caused by the cumulative effect of multiple inherited abnormalities that interact with each other and the environment to increase cancer risk.

The influence of other cancer-related genes may also explain why some patients with a BRCA1 or BRCA2 mutation develop breast, ovarian or other forms of cancer at a relatively young age, while other family members with the same mutation remains healthy throughout life.

In their normal form, the BRCA1 and-2 genes prevent breast cancer by producing a protein that controls cell growth. When someone inherits a BRCA1 or BRCA2 mutation from his or her mother or father the cell will still function normally if the normal gene copy inherited from the other parent is working properly. However, when the normal BRCA gene breaks down, for whatever reason, both copies of the gene are now abnormal and it can no longer control cell growth to prevent cancer. When breast cells multiply at a rate much higher than normal, some can invade healthy tissue and cause invasive breast cancer. This form of cancer differs from non-invasive cancer where cells also grow uncontrolled, but have not started to invade the normal surrounding healthy tissue.

In addition to diagnostic applications, several genetic tests became available during recent years for breast cancer prognosis and prediction of treatment response. Identification of genetic abnormalities may form the basis of intensified surveillance programs and personalized treatment programs. Genetic counselling is important to determine the appropriateness of genetic testing based on family history (e.g. BRCA1/2), pathology (e.g. MammaPrint) and environmental factors that may influence treatment response at the pharmacogenetics or nutrigenetics interface.

The Breast Cancer Gene-screen involves a comprehensive evaluation of breast carcinoma using a pathology supported genetic testing (PSGT) approach to define cancer subtypes, predict disease recurrence and guide treatment decisions. All breast cancers are caused by genetic abnormalities (mutations), which are either inherited or acquired.

A multi-gene DNA test can routinely be added to assessment of:

  • blood cholesterol and
  • glucose levels,
  • blood pressure and
  • body mass index (BMI) as part of Wellness Programs offered by healthcare practitioners.

It includes analysis of variation in clinically useful genes that may contribute to:

  • abnormal cholesterol levels,
  • homocysteine accumulation,
  • blood clotting,
  • iron overload and
  • inflammation.

Some of these abnormalities contribute to the development of type II diabetes, obesity and hypertension. Oxidative stress, detoxification of carcinogens and oestrogen exposure are also important considerations in this context.

This pathology supported genetic test is performed in conjunction with assessment of any food allergy or intolerances known to be associated with many chronic disorders. The results of the genetic test are combined with clinical indicators and lifestyle factors to identify a combination of risk factors that may lead to disease development or progression, if left untreated.

The initial medical consultation at Health Renewal will be approximately 45 minutes. As this is a prolonged medical consultation, the initial consultation fee will be R 975 (for non-loyalty members). On arrival you will have to complete an in depth questionnaire before the consultation so please arrive 20 minutes before the time. During the 45 minute consultation your Health Renewal doctor will obtain a FULL medical history from you to determine your personal risk. A physical examination will be done after which he/she will decide which blood tests need to be requested from your local pathology laboratory. If you have a medical aid, these should be able to be claimed as well.

Once we’ve received your results, they will then be analyzed by your Health Renewal doctor who will begin working on a unique prescription plan for you with the compounding pharmacy. At your pre-scheduled second appointment 2 weeks later, the results and examination findings will be discussed with you. This will determine what abnormalities/ deficiencies exist and you will be advised on your treatment options. These options may range from prescription medications, nutraceuticals, bio-identical hormonal creams / tablets or alternatively to having bio-identical implants / pellets inserted.

In office treatments such as carboxytherapy may also be recommended for certain conditions such as hair loss, erectile dysfunction (ED), menopause or PMS. If you need to lose weight our Body Renewal Medical Weight loss program may be recommended. All these recommendations will be summarized on a sheet / print out which you can take home with you. The nutraceuticals offered at Health Renewal are of superior quality (Solgar) and are not rancid nor contain Hg(mercury) or PCB'S (very important for Omega-3 essential fatty acids EFA’s). They are also free of gluten, preservatives, Wheat, Dairy, Soy, Yeast, Sugar, Artificial Flavour, Sweetener and Colour. We have a great professional team made up of doctors, trained and registered nurses and therapists to support you at any time. An added bonus is that not only improving your health and well-being, any nutraceuticals purchased will go towards loyalty points at any Skin, Body and Health Renewal branches.

1. You are kindly requested to bring any supplements that you are currently taking, along to your consultation. The doctor can check the ingredients in take this into account when prescribing a treatment plan for you.

2. Also, if you have had any blood work done in the past 6 months, please bring the results along to the consultation. Should you not be in possession of the hard copies, please request these results from the lab you visited. Usually your ID number is sufficient.

Depending on the exact prescription given, you may be required to return to the doctor within 1-4 months’ time, in order to ensure optimum hormone levels are achieved. This will be determined by a repeat blood test and may be requested by your Health Renewal doctor.

You should ensure that you are current with your gynaecological visits/breast exams/mammograms (for female patients) and prostate exams (for male patients) as recommended by your GP/gynaecologist.


The fee for the initial consultation and evaluation of 45 minutes is R975. A deposit of R400 is required up front in order to secure your consultation with the doctor. This advance payment goes towards your consultation fee. Proof of payment needs to be received one week in advance of appointment email. Please see banking and contact details below. This consultation fee may be claimed back from your medical aid depending on which kind of medical over you have.

A second follow up consultation is essential in order for the doctor to assess your blood work and prescribe a personalised treatment plan for you. Another deposit of R400 will be required to secure the second consultation.

All subsequent follow up consultations with the doctor will be charged at R650 for 30 minute consultations. This may be amended from time to time at the practice’s discretion.

You may pay for your consultation by cash, credit card or EFT.

BIHRT prescriptions must be paid for prior to ordering, as each patient’s prescription is unique to his/her own needs, and you will receive an invoice advising you of the cost.

The patient is responsible for paying all consultation and prescription fees to Skin, Body and Health Renewal – regrettably we do not accept medical aid.

An added bonus is that not only improving your health and well-being, any nutraceuticals purchased will go towards loyalty points at any Skin, Body and Health Renewal branches.

The importance of early management of any condition cannot be overstated. Once certain conditions set in and damage to organs occurs, complete recovery may be difficult to attain. Best results for prevention and longevity is early detection of a possible problem combined with conventional treatments, nutritional supplements and a healthy diet and lifestyle.

Some days you need some help staying motivated to live a healthy lifestyle. Our compilation of health and wellness quotes and sayings provide the inspiration or the laugh you need to keep making positive choices for your overall wellbeing.

Here are ten quotes from great thinkers to challenge, motivate and inspire us to exercise, eat right and live healthier lives: Health and intellect are the two blessings of life.

  • We must turn to nature itself, to the observations of the body in health and in disease to learn the truth.–Hippocrates
  • In the book of life, the answers aren’t in the back.–Charlie Brown
  • The difference between the impossible and the possible lies in a person’s determination.–Tommy Lasorda
  • If you don’t have confidence, you’ll always find a way not to win.–Carl Lewis
  • "The only way to keep your health is to eat what you don't want, drink what you don't like, and do what you'd rather not."Mark Twain
  • "The longer I live the less confidence I have in drugs and the greater is my confidence in the regulation and administration of diet and regimen."John Redman Coxe
  • "Poor health is not caused by something you don't have; it's caused by disturbing something that you already have. Health is not something you need to get, it's something you have already if you don't disturb it."Dean Ornish
  • "Those who think they have not time for bodily exercise will sooner or later have to find time for illness." Edward Stanley
  • "So many people spend their health gaining wealth, and then have to spend their wealth to regain their health." A.J. Reb Mater
  • "To avoid sickness eat less; to prolong life worry less." Weng Chu Hui.


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