Someone with CLL tell me experience of green tea and polyphenols

I am Japanese CLL patient, so I am sorry that my English is poor. I was diagnosed this year and stage A. My WBC is increasing at the rate of 1000~1500/month, and up to 27500 one month ago. So, I started to take concentrated green tea and polyphenol tablets (corresponding to several cups of tea; probably taking 500~600mg polyphenol every day). Fortunately, WBC decreased to 25500 in 1 weeks. However, the WBC again increased up to 26500 next week. So I increased dose (corresponding to 10 cups of green tea; may be 1000 mg polyphenols (approximately 500~600 mg EGCG contained). 1 week later, WBC count decreased to 23500. However, WBC increased up to 24500 next two weeks later. I expected that the effects of green tea continue at least several months. Unfortunately, green tea and polyphenol tablets seem to affect only 1~2 weeks in my case. The dose of polyphenol may not be enough. I do not want to take high dose of polyphenols, because it is not good for liver. Anyone have such experience? Please anyone tell me experience of green tea, polyphenol tablets. I hope to hear experiences who improved CLL by taking green tea extracts.


32 Replies

  • Hi Miee,

    Your English is very good and you've clearly explained what you want to know.

    There are two important points you need to understand:

    1) Haematologists don't worry about changes in WBC (more correctly ALC - Absolute Lymphocyte Count) until the ALC climbs above 30 (or 30,000 in your units).

    2) The variations in your WBC are most likely unrelated to your green tea consumption as you probably aren't taking a high enough dose. You may also fall into the minority of patients that don't see a benefit from green tea. The best way to work out if green tea is having an effect, is to compare your WBC average now (say over three or more blood test results) with what it was before you started taking the green tea (again over three or more results). Also, you should be looking at the overall trend in your WBC over many months, not looking at month to month changes. Finally, your WBC is only a small part of your tumour burden. Most of it is typically in lymph nodes and at later stages, your spleen and bone marrow. The green tea may also be reducing the size of your lymph nodes, which you can't easily determine without a CT scan comparison, unless you have some prominent nodes typically around your neck, in your armpits or in your groin.

    Here are a couple of earlier posts on EGCG which include information on the liver tests you need to watch.

    Have a read and please ask if you have any more questions.


    PS Do you live in Japan? If so, have you found a good CLL specialist? I'm asking because CLL is fairly rare in the Asian population, perhaps because green tea is so popular there :) .

  • Hi Neil

    Thank you so much for a prompt response. In Japan, we have only 1000~2000 CLL patients. I guess that we have few CLL specialists, so I want to collect informations on CLL.

    You wrote that green tea extract (EGCG) reduced size of lymph nodes . I also know because I read paper on phase II test of EGCG. I wish to know whether reduction of lymph nodes may continue, or it is temporary (again lymph nodes size increase despite continue to have EGCG ), if you have any information.

    Finally, I appreciate if you could suggest me the best way to delay progress of CLL.

  • Miee, since you've read the Mayo Clinic Phase II trial paper, you know as much as I do about the long term use of EGCG. Sadly, Mayo Clinic haven't done a follow-up study on how the patients on that trial have fared. That's probably because:

    (a) The Phase II trial funding came from donations provided to CLL Topics/Updates, who went out to tender for a CLL research group to do the trial and Mayo Clinic got the work. There were plans for a Phase III study, but it didn't happen.

    b) The supplier of Polyphenol E (the EGCG formulation used by the trial participants) ceased providing Polyphenol E for CLL research. I understand some trial participants continued on with other sources of EGCG, but that was uncontrolled, making any follow up research of limited use.

    As with other cancer treatments, it is reasonable to expect that CLL clonal evolution will result in EGCG becoming less effective over time. There are a number of different cell pathways disrupted by EGCG in CLL cells, so that may minimise the chances of clonal evolution developing, but we just don't know. I alternate taking EGCG with turmeric for that reason (trying to prevent clonal evolution), but that is purely something I am doing with minimal scientific research supporting that approach.

    As to the best way to delay the progress of CLL, I wish I knew! Obviously getting the right CLL markers (like choosing your parents) works well :) . Seriously, all I can suggest is that you help your body fight progression by eating a wide range of healthy foods, get/keep fit, try to avoid infections and keep your weight in a healthy range and perhaps try a supplement like EGCG, where there is a scientifically proven benefit for a significant percentage of CLL patients. Just make sure you let your medical team know what you are taking so that they can monitor your liver function and advise you when you should stop taking a supplement if you are prescribed a drug which is not compatible with the supplement.


  • Hi Neil:

    Thank you so much for many informations.

  • Hi Neil:

    I have one question. In your case, Do EGCG and turmeric improve your CLL?


  • Miee, one of the frustrations with CLL is that it varies so much between individuals and within an individual over time. That makes it very hard to say on the basis of my experience whether what I've spent a great amount on over the years has done me any good. It is also why people with CLL are so easy to convince that some alternative treatment is doing them good. That's why the only way to really test potential treatments out is by trials with a significant number of patients on the trial.

    Having said the above, it was an investigation into quickly worsening neutropenia that led to my SLL diagnosis almost 6 years ago. I got down to an ANC of 0.4 or grade 4 neutropenia which put me at severe risk of infection. My ANC recovered to grade 2 before I started on the EGCG and has gradually dropped to between grade 3 and 4 this year. My enlarged spleen hasn't become any more enlarged according to my haematologist and my lymph nodes aren't much bigger as far as we can tell. My once sceptical haematologist has told me to stay on the green tea capsules. But perhaps this is the path that my CLL would have followed without me taking green tea and turmeric? I've have mild arthritis in my hands - diagnosed by my doctor. I do find that the turmeric helps with that - well I think it does as I gather arthritis can come and go too. Anyway, it is quite some time since my hands have had any discomfort from arthritis. Turmeric is known for its anti-inflammatory properties; perhaps that's helped with the CLL too? But this is all conjecture on my part.

    From what little work has been done on turmeric and CLL, it is hard to see how high enough blood serum levels of the active ingredient can be achieved to have any positive effect on CLL. You'll see turmeric sold in various formulations, typically including black pepper/piperine to boost the absorption into the blood stream. Taking it with soy milk or a fatty meal is also supposed to assist the absorption.

    As Chris (Cllcanada) has warned elsewhere, in the majority of countries, supplement manufacture and sale is not regulated, so you don't know what strength dose you are getting or what other ingredients (some of which can be quite harmful) are included. In Australia the supplement industry is regulated and the regulating body can and does put companies out of business that do not have processes in place to verify what they sell in Australia matches the claimed ingredient quantities. I don't know what the situation is in Japan.


  • I totally agree... the problem I have with early quasi treatments is that it 'might' be picking off the low hanging B cells...

    New research has confirmed that CLL is an ever changing scene... when the weak B cells are gone in treatment ... the very agressive B cells take over...

    This is well documented by Catherine Wu and others...

    Know what you are doing... and do NOTHING without your doctor's approval.

  • Neil:

    Thank you so much for details. Turmeric, interesting.

    I have a chronic prostatitis for several years, and sometimes became worse. I guess that because it is a kind of inflammation, CLL will progress concomitantly. I will think about turmeric.


  • Miee, it is important that you don't try more than one thing at the same time or you won't know what is helping you.

    Further, turmeric and green tea have been shown to work better alternated rather than together against CLL. I alternate 5 days on green tea and two days on turmeric.

    The suffix ' itis' after an organ in English means 'inflammation of' that organ, but it could be dangerous to take something like turmeric in an attempt to treat your prostatisis without understanding the underlying cause of the inflammation.


  • Hi, I'm fairly new to all this having been diagnosed with CLL stage A in October with a low count (whatever that might mean), anyway I too asked about Green tea & dosages. In the replies I received it seemed those taking it are on anything from 1000mg up to 3000mg, although it was generally recommended that I should discuss with my Dr, because of the potential problem with liver damage. I'm currently taking 350mg tablets & will discuss further with my Dr when I next see him in April, to see if they have any advice on this topic & whether I should get closer to the dosage the used in Mayo Phase 2 which seems to be 2000mg.

    From the many posts I have read & what the Dr's have told me, staying generally fit & health, exercising regularly, avoiding bad doses of the flu, shingles or other infections seem to be the best way of trying to slow the progress of the condition down.

  • The dose in the Mayo Phase two was 2000 mg of PolyphenonE twice a day.

    However, you need your doctor to monitor your liver on a regular basis...EGCG in these doses can cause liver problems...

    Dr. Neil Kay one of the trial docs no longer recommends the use of over the counter supplements of EGCG, because quality varies and nobody knows for certain the dose or adulterations or toxicities...

  • Thanks, it's why I want to talk to my Dr before upping my dosage.

  • Thank you for reply. I am also afraid that high dosage of EGCG may cause liver damage. So I do not want to increase.


  • Hello Miee,

    Just a few more ideas re delaying the progress of CLL...

    I've heard that anything that causes inflammation in your body, can make CLL get worse. This could be allergies like hay fever, being overweight, asthma, infections, any foods that your body doesn't react well to, things that irritate your guts or skin, etc. So it's worthwhile trying to avoid these sorts of things.

    As others have already said, anything that improves our general health is good - like exercise, eating well and avoiding infections. It's a good idea to keep up with any vaccinations, especially in the early stages of the disease, because as it gets worse, our bodies are less capable of producing the helpful antibodies from vaccinations. Check with your doctors though, re which vaccinations are safe for people with CLL. ("Live" vaccines such as the one for Shingles are NOT recommended).

    Best wishes,


  • iHi Paula:

    Thank you a lot of things for delaying CLL. I have an inflammation in my body now. I have to cure this.


  • If you can purchase PolyphenonE from Mitsui Norin it might be worth trying, under your doctor's supervision... otherwise I would forget it...

  • Hi Cllcanada:

    Yes, my polyphenol tablets from Mitsui Norin. Are You also taking polyphenol? If so tell me the effects of it.


  • Polyphenon E was available in Canada and there was a product called Can-Tea a green tea lozenger... but they are no longer produced.

    I never used them...

  • 4 g EGCG ( we buy it from Healthy Origins TEAVIGO brand more than 90 % purity ) + 8g Curcimin C3 complex with bioperine + 10000 units Vitamin D3 .Response seems to be dose dependent

  • Hi ikahan:

    Thank you for interesting informations. Anyway, do you taking these doses every day?

    How long have you been taking? Does your CLL progression speed decrease or stop?


  • Yes, my husband takes these doses every day. These are the doses used per day in the MAYO clinical trials. Also a diet rich in soy products { rich in genistein ) and 6 ounces watercress ( rich in phenyl isothiocyanates ). He started 3 months ago when he was diagnosed. We don't know yet how well it works.


  • Thank you for a reply. Please tell me if you will find effects of diets. I expect that ALC count of your husband will decrease.


  • Interesting discussion. I've had CLL for 12+ years. My ALC hovered around 280 with a 4-year doubling time for quite a while -- about a year at least. I had no problems until breaking 3 ribs; apparently the healing process increased hypercoagulability, so at the 60-day mark I developed (in the context of the CLL) pulmonary emboli, leading to a 36-hr hospitalization & being placed on Lovenox/ enoxaparin self-injections.

    I was an early adapter of ECGC capsules at 4,000/d; in regard to the question of whether this would provoke gall bladder issues, I placed myself on a daily liver/ gall-bladder cleansing tea. Once MD Anderson clinic grabbed hold of the Mayo clinic start of using EGCG and then added curcumin, I followed suit taking 1,500mg/d; when they then announced that adding quercetin to the EGCG, I followed suit taking 1,500mg/d; when they then determined that alternating the EGCG/ quercetin doses with the curcumin doses was the ideal approach in terms of provoking/ supporting apoptosis, again I followed suit.

    Response? Like others have said, I've had next to zero EXTERNAL lymphadenopathy until a small lump appeared low on my neck about 6 months ago. Also, the ALC didn't seem to be increasing very rapidly -- but there is HUGE variation in all this among patients. I've been worked up at now 4 different CLL centers, and a common comment has been about my relative lack of EXTERNAL lymphadenopathy.

    After the above noted episode of pulmonary emboli secondary, probably, to hypercoagulability, it was decided that I go a round of 4 infusions of rituxamab over a 23-day period -- and to consider repeating this (or something similar) in the future if the ALC hits about 225 (rather than the 285 where it had been for so long -- before jumping to 370 during the pulmonary emboli "reactive lymphocytosis" state). Obviously the CT and MRI scans picked up INTERNAL lymph nodes all over the place; the most notable change after rituxamab was the improvement in gastrointestinal tract function -- suggesting that there must have been INTERNAL lymph nodes impinging on this and that.

    I guess I'm voting in favor of following the EGCG/ quercetin alternating with curcumin/ peperine protocol more or less outlined by Mayo & MD Anderson investigators. (Don't forget the liver/ gall-bladder cleansing tea.) It is easy enough to argue that this protocol might have some positive impact on overall health.

    Oh -- I've also been on relatively high-dose phosphodiesterase inhibitors across the years -- mostly to target pdei4 and pdei7 -- again, toward provoking ing/ supporting apoptosis but that's another story, maybe covered somewhere else on this blog.

  • 70s-80s-overlander

    Thank you for very interesting story. I hope that you will post on PDE inhibitor story. Recently Japanese scientist and colleagues found that a combination of EGCG and PDE inhibitor extremely killed CLL cells cultured in petri dishes. Which kinds of PDE inhibitors did you have? Sildenafil? Did you have a combination of EGCG and PDE inhibitor (at the same time)? In your case, was it effective for suppressing CLL progression?


  • I have been on pentoxifylline (mostly a pdei4) almost from the beginning 12 years ago, as one of my first issues was retinal arteritis, probably related to CLL-induced hyperviscosity. 9 years ago the dose was increased from the standard 1,200mg/d to the known-safe dose of 2,400mg/d.

    Since the most common cause of death in CLL remains pneumonia -- and since the EARLIEST indication that phosphodiesterase inhibition somehow helped CLL was the French observation that some CLL patients taking theophylline (mostly a pdei3) for asthma had a better CLL course, I also have been on theophylline from the beginning 12 years ago. About 9 months ago the dose was raised -- carefully -- from the usual maximum dose of 900mg/d to a split-up dose of 450+100+450+100 -- for a total of 1,100mg/d -- and my trough blood level still was on the low side, ie, safe.

    About 4 or 5 years ago I began tadalafil 5mg (mostly a pdei5). By now, ALL so-called "erectile dysfunction" (ED) meds (quite expensive in the US) have been demonstrated to have apoptotic effects in CLL.

    About 6 months ago I began sildenafil 20mg (mostly a pdei5) -- the recommended dose for pulmonary hypertension (and less expensive than the ED dose) -- especially since I have had mild pulmonary hypertension for years. [Extra note: CHILDREN with malaria get pulmonary hypertension from the increased blood viscosity -- so it comes as no surprise that this condition might appear in CLL. For most of the 12 years I've treated this -- just like the malaria kids are treated -- with L-arginine 1,000 tid.]

    Most pharmacists comment along the lines of, "That's a lot of pdei!" I've had NO problems with the combination of meds that were added one by one by one.

    Yes, I've taken the phosphodiesterase inhibitors virtually the entire time I've taken the EGCG/ quercetin alternating with curcumin/ peperine. I always checkout the maximum dose data and toxicity data on ingredients -- and there are SOME data on the combinations -- so, with my docs have "veto power" on the ideas we've proceeded slow and carefully. I got to 12+ years without any iv therapies -- and with close to no EXTERNAL nodes -- but who knows how I would have done without this "daily approach to treating CLL". Again, the data -- especially on pentoxifylline -- as being helpful in a zillion medical conditions once again makes it easy enough to argue that this protocol might have some positive impact on overall health.

    If you haven't found the website already, please let me recommend -- the US government's FREE database of the world's medical literature in abstract -- with a number of abstracts also having the full FREE article on that US government website. Below is the PubMed abstract of the article you mentioned. Vardenafil, at least in the US, is the MOST EXPENSIVE pdei out there.

    Br J Haematol. 2015 Feb;168(4):610-3.

    "Vardenafil, a clinically available phosphodiesterase inhibitor, potentiates the killing effect of EGCG on CLL cells."

    Kumazoe M, Tsukamoto S, Lesnick C, Kay NE, Yamada K, Shanafelt TD, Tachibana H.

    I wish you the best.

  • Thanks for your detailed and interesting summary of your experiences.

    The full article of the paper you referenced is available free from the Wiley site.

    Click on any of the Get PDF (418K) instances on that page.


  • 70s-80s-overlander, Neil

    Thank you so much for a detail. I have read this article. In experiments using CLL cells cultured in petri dishes, a combination of EGCG and PDE inhibitor have excellent results.


  • Our clonal (cancerous) B-CLL cells are fragile and easy to kill in a test tube (in vitro) with a wide range of substances. (That's why it is so common to see 'smudge cells present' comments on blood test results.) The difficulty comes in proving that something that works 'in vitro' also works 'in vivo' or in your body. There's a lot of science in working out the best way to achieve a high enough blood concentration of the 'in vitro' active substance 'in vivo' to have any clinical effect. Do you inject or deliver the substance orally? How do you prepare the substance so that it survives the digestion process and is absorbed into the blood stream? Can you be sure that the substance isn't neutralised by your body or that affected B-cells aren't able to engage assistance to overcome the effects of the substance? That's why we need properly conducted clinical trials...


  • Neil


    Thank you for your experience and valuable comments on in vitro and in vivo experiments. I understand very well what Neil wrote. I am a scientist working on intracellular signal transduction, so I have many experiences on difference between in vitro and in vivo experiments. I have done experiments using PDE inhibitor, so I was quite interested in a signaling pathway inducing apoptosis of CLL cells that is activated by 67 kDa EGCG receptor (cell surface receptor). I believe that clinical EGCG effect is probably mainly due to an apoptosis of CLL cells through 67 kDa EGCG receptor, because EGCG affects cell surface receptor (in other cases of inhibiting intracellular target molecules, much more higher plasma EGCG concentration is needed) . This pathway is strongly enhanced by PDE 5 inhibitor such as vardenafil. Vardenafil is now clinically used in other therapy and its effective concentration for inhibiting PDE 5 is not harmful. Now we know that EGCG is clinically effective for CLL and vardenafil also effective in other therapy, and they are basically safe (although high concentration of EGCG has several side effects). Unfortunately, we do not know whether or not a combination of EGCG and vardenafil may be safe. That is why I asked informations if someone have tried to take a combination of EGCG and PDE 5 inhibitor, because clinical trial will be many years later. I guess that even mouse experiments have not been completed.


  • I think we all agree that controlled IN VIVO experiments would be ideal. In the meantime I vote for working with a doc who is willing to make an intelligent decision about how to work within the safe parameters of relatively well-known medications. Yes, high-dose EGCG should be avoided with pregnancy and might impact platelets -- but we sort of know what kind of a "high dose" is safe for most people. Yes, high-dose curcumin can provoke gall-bladder issues -- but we sort of know what kind of a "high dose" is safe for most people. Yes, high dose theophylline can cause stomach irritation and fast heart beat -- but we sort of know what kind of a"high dose" is safe for most people. Etc, etc, for quercetin, pentoxifylline, tadalafil, sildenafil, vardenafil, vitamin D, etc, etc. What we DON'T know, of course, is what happens when all these are mixed. We have SOME data on some of the mixings -- but nowhere near as much data as we would like. This is true for almost every area of medicine.

    I posted my experience over the last 12 years because during those years I had an intelligent hematologist and an intelligent internist -- plus access to a pulmonologist, an immunologist, a cardiologist, an endocrinologist, an otolaryngologist, etc, etc. The internist and I were in the center. Everyone had veto power. We were trying not to do anything that obviously would be stupid. It was fantastic when the Mayo and MD Anderson clinics started checking out these approaches -- as they, too, were not trying to do anything stupid. We can "watch and wait" -- but that made a bit more sense when the average CLL patient was in the 70s or 80s or 90s. Now that we have 35 year old CLL patients, it's a whole new world. [I was 54 years old at time of diagnosis.]

    “if no randomized trial has been carried out for our

    patient's predicament, we must follow the trail to the

    next best external evidence and work from there.”

    Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS.

    “Evidence based medicine: what it is and what it isn't.”

    Brit Med J. 1996 Jan 13;312(7023):71-2, p.72.

    I'm hoping to hear from some other folks who have gone the EGCG/ quercetin/ curcumin route -- or the phosphodiestersase inhibitor (PDEI) route -- or, like me, combined both. The article noted above openly combined the two, but it was an in vitro rather than in vivo study. [I guess that makes me an in vivo study of one.]

    [We know that pdei7 appears to be the most anti-CLL -- but the only pdei7 med currently available is too toxic. A number of safe pdei meds, however, SOMEWHAT hit pdei7 -- and thus comes the idea of combining several of those "close but not quite" meds. Next in line after pdei7, in terms of anti-CLL activity, appears to be pdei4; then comes pdei5. There must be an answer in there somewhere -- or nearby. Need I add that all these pdeis are relatively inexpensive compared to other treatments for CLL?]

  • The median age at diagnosis for CLL was 72 years in 2000 , now SEER data says 71 yo, the Germans use a 69 year median... the demographics haven't shifted much... I was 52 at diagnosis in 1998...

    Same world.. just looks different on the internet...

  • The study out of Mayo Clinic now is a year and a half old, but it suggests that early-onset (before age 55) CLL has some specific issues. "As a collective group, the median overall survival of CLL patients aged ≤55 is 12 years - which is significantly shorter than that of the age- and sex-matched population. Despite this discouraging group average, we found that approximately 25% of young patients in our study who have Rai Stage 0 disease and either mutated IGHV genes or a favorable FISH risk category (such as normal cytogenetics or 13q-) have a survival comparable to that of the age- and sex-matched general population."

    "median overall survival of ... is 12 years" -- but one-fourth of those in the early onset group do fine.

    Most of my elders lived into their 90s and a number made it to 100. Getting CLL at age 54 certainly suggested that I'd need to have a "Plan A" regarding living to about age 66 or so, and a "Plan B" regarding living to age 95 or so. For me that meant that maybe my life's work would be cut short by about 30 years -- and that I'd best get my family better situated to handle an early demise.

    Getting CLL at age 55 or younger is a very different phenomenon from getting CLL at age 75 or older. Those with early onset CLL have more of an incentive to push research and less of an incentive to "watch and wait" -- which, for years, was a standard treatment for the those likely in the last decade of life.


    Sameer A. Parikh, Kari G. Rabe, Neil E. Kay, Timothy G. Call, Wei Ding,

    Susan M. Schwager, Deborah A. Bowen, Michael Conte, Diane F. Jelinek,

    Susan L. Slager, Tait D. Shanafelt

    "Chronic lymphocytic leukemia in young (≤ 55 years) patients:

    a comprehensive analysis of prognostic factors and outcomes."

    Haematologica January 2014 99: 140-147.

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