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Green Tea and Cancer September 5, 2018

Posted by Dreamhealer in best vancouver naturopath, Cancer, cancer prevention, cancer therapy, Cancer Treatment, Chemotherapy, Healing, integrative cancer care, naturopath, naturopathic, Naturopathic Doctor, Naturopathic Medicine, naturpathic medicine.
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Written By: Dr. Adam McLeod, ND, BSc (Hons)

Green tea is a common beverage that can be found at any cafe yet it also has important therapeutic properties.

Epigallocatechin gallate (EGCG) is an extract from green tea that has shown great promise as an integrative cancer therapy. The mechanism of action is complicated because it interacts with multiple molecular pathways to inhibit the growth of cancerous cells. When cancer cells are exposed to EGCG, it triggers cell death by a variety of mechanisms1,2,3,4. Not only does it inhibit the growth of cancerous cells, but it also slows down the rate of metastasis.

Although there is a wide range of EGCG content in green tea, a strong tea has about 70mg per tea bag. The therapeutic doses for EGCG (particularly in the context of cancer) is a minimum of 1500mg per day. Which means you would have to have approximately 20 green teas per day to reach this dose. Obviously this is not practical as a long term treatment plan so the best way to get the appropriate doses is through pill form. If you enjoy having green tea then you can certainly continue to do so but you will not be significantly contributing to the therapeutic effect of the EGCG.

One important characteristic of EGCG is that it acts as an anti-angiogenic substance. Angiogenesis is the growth of new blood vessels into a developing tumour. This process is necessary when cancer cells are spreading because the smaller growths need a blood supply to sustain their rapid growth. Cancer cells will often secrete chemicals that trick the human body into growing blood vessels into the tumour. EGCG helps to inhibit this process by inhibiting the viability of capillary tube formation and migration. This effect seems to be greatly enhanced by a new class of drugs called ERK inhibitors2.

Tumour samples of mice treated with EGCG clearly show that the cancerous cells have reduced ERK activity while having enhanced p38 and JNK activity. In other words, the pathways that promote growth are down-regulated and the pathways that inhibit growth are up-regulated. The net effect is that the cancer does not grow or spread as quickly. Every molecular marker that was tested indicated that the cancer was less aggressive and more prone to cell death. If you perform a quick Google scholar search, you will see hundreds of well-controlled studies that consistently demonstrate this anti-cancer effect.

When EGCG is combined with curcumin at high doses, it helps to stabilize leukemias and lymphomas. There are many well-documented cases of patients with multiple myeloma who have had long-term disease stabilization by simply taking high doses of EGCG and curcumin. These natural compounds work synergistically to reduce inflammation and promote cell death in cancerous cells. The effectiveness of EGCG in multiple myeloma is undeniable, and this has resulted in a resurgence of research into its use as an adjunctive cancer therapy6.

There are a handful of chemotherapy drugs where the use of EGCG is contraindicated such as bortezomib (Velcade). There is contradictory information about the significance of this interaction, but it is still best to avoid combining EGCG with velcade15. Some doctors focus on this one interaction while ignoring the overwhelming evidence that EGCG often acts synergistically with other forms of chemotherapy. It is difficult to argue against the use of EGCG if you take the time to actually look at the evidence. When EGCG is combined with cisplatin, it not only significantly increases the effectiveness of the drug, it also dramatically reduces the side effect profile7,8,9.

Recently in the media, concerns have been raised about the connection between EGCG and liver toxicity. These liver toxicity reactions that are potentially related to EGCG are exceptionally rare considering how regularly EGCG is consumed in the general population. There have been several documented case studies of liver toxicity that have been connected to use of EGCG. It appears that there may be a genetic predisposition to these rare reactions12. At this point in the time mechanism of action for these reactions is unclear, however, it is in many cases likely due to a immune-allergic mechanism. In other words, it could be that some of these patients were just simply allergic to EGCG.

There is contradictory information regarding the impact of EGCG on liver as several animal studies indicate that it actually has a strong protective effect on the liver and kidneys10. I can tell you from experience that I have literally prescribed EGCG thousands of times and I have never seen even a hint of such reaction. EGCG is a exceptionally safe supplement when used appropriately and patients should not be fearful of using it due to a handful of exceptionally rare cases of liver toxicity.

EGCG is an example of a supplement where the quality makes a significant difference. In order to obtain the desired anti-cancer effect, you must take high doses of quality EGCG. Drinking green tea may be helpful in the context of cancer prevention, but when it comes to cancer treatment, you need much higher doses. Some physicians recommend that patients get EGCG administered by intravenous therapy to get the doses as high as possible. The doses required to enhance chemotherapy and promote cell death in cancerous cells are quite high, but they are obtainable by consuming EGCG orally. It is also important to point out that this treatment is cost effective and generally well tolerated by patients.

Dr. Adam McLeod is a Naturopathic Doctor (ND), BSc. (Hon) Molecular biology, Motivational Speaker and International Best Selling Author. He currently practices at his clinic in Vancouver, British Columbia where he focuses on integrative cancer care, providing the best care in integrative oncology. http://www.yaletownnaturopathic.com

Dr. McLeod will be holding two seminars in 2018, Vancouver, British Columbia and Toronto, Ontario. For more information on his seminars please visit the website: http://www.dreamhealer.com/workshop/


1) Ahmad, Nihal, Sanjay Gupta, and Hasan Mukhtar. “Green tea polyphenol epigallocatechin-3-gallate differentially modulates nuclear factor κB in cancer cells versus normal cells.” Archives of biochemistry and biophysics 376.2 (2000): 338-346.

2) Shankar, Sharmila, et al. “EGCG inhibits growth, invasion, angiogenesis and metastasis of pancreatic cancer.” Frontiers in bioscience: a journal and virtual library 13 (2007): 440-452.

3) Hwang, Jin-Taek, et al. “Apoptotic effect of EGCG in HT-29 colon cancer cells via AMPK signal pathway.” Cancer letters 247.1 (2007): 115-121.

4) Shimizu, Masahito, et al. “EGCG inhibits activation of HER3 and expression of cyclooxygenase-2 in human colon cancer cells.” Journal of experimental therapeutics & oncology 5.1 (2004): 69-78.

5) Shah, Jatin J., Deborah J. Kuhn, and Robert Z. Orlowski. “Bortezomib and EGCG: no green tea for you?.” Blood 113.23 (2009): 5695-5696.

6) Shammas, Masood A., et al. “Specific killing of multiple myeloma cells by (-)-epigallocatechin-3-gallate extracted from green tea: biologic activity and therapeutic implications.” Blood 108.8 (2006): 2804-2810.

7) El-Mowafy, A. M., et al. “Novel chemotherapeutic and renal protective effects for the green tea (EGCG): role of oxidative stress and inflammatory-cytokine signaling.” Phytomedicine 17.14 (2010): 1067-1075.

8) Davenport, Andrew, et al. “Celastrol and an EGCG pro-drug exhibit potent chemosensitizing activity in human leukemia cells.” International journal of molecular medicine 25.3 (2010): 465-470.

9) Sarkar, Fazlul H., and Yiwei Li. “Using chemopreventive agents to enhance the efficacy of cancer therapy.” Cancer Research 66.7 (2006): 3347-3350.

10) Niu, Yucun, et al. “The phytochemical, EGCG, extends lifespan by reducing liver and kidney function damage and improving age‐associated inflammation and oxidative stress in healthy rats.” Aging Cell 12.6 (2013): 1041-1049.

11) Chen, Ju-Hua, et al. “Green tea polyphenols prevent toxin-induced hepatotoxicity in mice by down-regulating inducible nitric oxide–derived prooxidants.” The American journal of clinical nutrition 80.3 (2004): 742-751.

12) Church, Rachel J., et al. “Sensitivity to hepatotoxicity due to epigallocatechin gallate is affected by genetic background in diversity outbred mice.” Food and Chemical Toxicology 76 (2015): 19-26.

IBS – But What CAN I Eat? May 12, 2016

Posted by Dreamhealer in best vancouver naturopath, best vancouver nutritionist, Diet, Healing, Naturopathic Doctor, Naturopathic Medicine, naturpathic medicine, stress.
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Written by: Breanne Dunlop, RHN

Suffering from abdominal pain, cramps, bloating, and gas? You’ve likely been told it could be IBS. Irritable bowel syndrome is the diagnosis often given to people who suffer from uncomfortable symptoms regarding the gut and bowels, and is distinct from Irritable Bowel Disease as the cause of irritation is unknown. IBS as you can imagine is extremely uncomfortable for those who suffer from it. Symptoms can be chronic or sporadic but are typically triggered by certain foods or during periods of stress. Some individuals are more prone to constipation while others may experience diarrhea. Whether you are chronically dealing with gut pain or have anxiety about being out in public during a flare up, IBS can be very crippling for many of its sufferers.

Since the cause of irritation is unknown and is likely different for everyone, the remedies to help provide some relief will be different too. The only sure way to know what may help you is through trial and error. Food is meant to be therapeutic and nourishing but for IBS sufferers it can be a nightmare trying to figure out what you can tolerate and what brings you agony. Right now there are three diets recognized to help with IBS: SCD, FODMAP or GAPS.

Specific Carbohydrate Diet (SCD) is a whole foods diet that avoids processed foods, sugars, starches and grains. The belief here is that complex carbohydrates are slow to digest and the pathogens bad little critters in our gut feed off of them. Only monosaccharides (simple sugars) are permitted on this diet as they are easier on the digestive tract. When food is properly digested and absorbed, there is nothing left in the gut for the bad little critters to feed on.

FODMAPs stands for Fermentable Oligosaccharides Disaccharides Monosaccharides and Polyols and aims to starve the bad bacteria by limiting foods that are poorly absorbed in the small intestine. FODMAPS has been further researched since SCD was introduced and therefore limits more foods (including monosaccharides) that are now known to be troublesome for an irritated gut. Foods are rated as low, medium or high FODMAP and the goal is to limit as much as possible high FODMAP foods because when eaten in excess these foods feed pathogens in the gut.

Gut And Psychology Syndrome (GAPS) is more restrictive than the previously mentioned diets, especially in the introductory phase. GAPS has more of a therapeutic approach to heal the gut versus just eliminating foods that are causing damage. The introductory phase, which lasts three to six weeks, consists entirely of homemade meat stock and vegetables with added probiotic rich foods such as sauerkraut – so hopefully you love soup!

Tired of suffering with your IBS? A holistic nutritionist can provide guidance on how to successfully eliminate trigger foods and incorporate foods and supplements that will help repair and nourish your gut. No more gut pain = a healthier and happier you. Book an appointment with Breanne today for assistance on how to implement one of the above diets into your lifestyle.

Diabetes Drugs for Cancer? September 24, 2015

Posted by Dreamhealer in Cancer, cancer therapy, Diabetes, Naturopathic Doctor, naturpathic medicine.
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Diabetes drugs
Written by: Dr. Adam McLeod, ND, BSc (Hons)

Can drugs traditionally used for diabetes also be helpful with cancer? There is a growing body of evidence which indicates that both Metformin and a class of drugs known as thiazolidinediones can be a useful adjunctive cancer therapy. The biochemical mechanism behind this anticancer effect is poorly defined but there are some intriguing theories about the mechanism of action.

Metformin is the first line drug for patients with Type 2 diabetes and it is certainly effective at getting the blood sugar under control. Diabetic patients who regularly take metformin have a lower risk of developing cancer1. Metformin activates an enzyme known as AMPK. A recent breakthrough has found a key regulator of AMPK to be a protein known as LKB1. LKB1 is a well recognized tumour suppressor. Activation of AMPK by metformin and exercise requires LKB1, and this would also explain why exercise is beneficial in the primary and secondary prevention of certain cancers2.

Recent studies strongly indicate that the anticancer effects of metformin are indeed linked to AMPK3. Metformin appears to selectively target cancer stem cells, and acts together with chemotherapy to block tumour growth and prolong remission4. When used with doxorubicin it acts synergistically to reduce tumour mass and relapse rates more effectively than either drug alone.

There is a completely different class of medications that is also used for diabetes which appears to have anticancer effects. The drug class is known as thiazolidinediones. One of the most well known drugs in this class is called Avandia. Even though both of these drugs are effective at treating diabetes they work by a completely different mechanisms. The thiazolidinediones activate a receptor called PPAR and by activating this receptor it triggers a cascade of reactions that are beneficial to patients fighting cancer6,7,8. The drug increases the activity of a key tumour suppressor called PTEN5. This tumour suppressor is a protein that halts the growth of cancer cells by inhibiting an enzyme known as PI3K. There are many types of cancer that are dependent on inhibiting the function of the tumour suppressor PTEN. The bottom line is that this drug helps to put the brakes on the growth of cancerous cells by activating PTEN.

As more research accumulates supporting the fact that these antidiabetic drugs can be used to treat cancer, one thing is becoming clear. The anticancer effect from these drugs is due to their influence on several different metabolic pathways. The great thing about these medications is that they have a long history of use and they are well established as safe adjunctive cancer therapies. Like any medication it has to be used in the right context and this therapy is not for everyone. A Naturopathic doctor who focuses in oncology will go through your entire case history to determine if this treatment is indicated. Contact your local naturopathic doctor to see if this therapy is right for you.

Dr. Adam McLeod is a Naturopathic Doctor (ND), BSc. (Hon) Molecular biology, First Nations Healer, Motivational Speaker and International Best Selling Author.
He currently practices at his clinic, Yaletown Naturopathic Clinic, in Vancouver, BC where he focuses on integrative oncology.

1) Evans, Josie MM, et al. “Metformin and reduced risk of cancer in diabetic patients.” Bmj 330.7503 (2005): 1304-1305.

2) Bauman AE.Updating the evidence that physical exercise is good for health: an epidemiologic review.J Sci Med Sport2004; 7:6–19.

3) Zakikhani, Mahvash, et al. “Metformin is an AMP kinase–dependent growth inhibitor for breast cancer cells.” Cancer research 66.21 (2006): 10269-10273.

4) Hirsch, Heather A., et al. “Metformin selectively targets cancer stem cells, and acts together with chemotherapy to block tumor growth and prolong remission.” Cancer research 69.19 (2009): 7507-7511.

5) Farrow, Buckminster, and B. Mark Evers. “Activation of PPARγ increases PTEN expression in pancreatic cancer cells.” Biochemical and biophysical research communications 301.1 (2003): 50-53.

6) Bunt, Stephanie K., et al. “Rosiglitazone and Gemcitabine in combination reduces immune suppression and modulates T cell populations in pancreatic cancer.” Cancer Immunology, Immunotherapy 62.2 (2013): 225-236.

7) Monami, Matteo, Ilaria Dicembrini, and Edoardo Mannucci. “Thiazolidinediones and cancer: results of a meta-analysis of randomized clinical trials.” Acta diabetologica 51.1 (2014): 91-101.

8) Srivastava, Nishi, et al. “Inhibition of Cancer Cell Proliferation by PPARγ Is Mediated by a Metabolic Switch that Increases Reactive Oxygen Species Levels.” Cell metabolism (2014).

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