Summer and Fall Supplement Plans

Now that I have had my June blood tests, I have begun my summer supplement experiment. A few months ago I ordered curcumin capsules without bioperine from a reliable company in Milan. So this summer I want to see if the no-bioperine capsules will work as well as the ones with bioperine that I have been taking since last fall. I won’t change anything else about my intake, which will still include quercetin and oil capsules, and an occasional folic acid pill. A quick note: my Italian curcumin capsules are much smaller than my U.S. ones. I checked their weight (following the example of my friend Don, please see his informative Myeloma Hope blog), and found it to be correct. Why make big capsules if smaller ones work just as well? Smaller capsules are much easier to swallow, so that would be another point in their favour, if they work.

In the fall, I plan to take on a more ambitious project. I have ordered Chinese skullcap capsules (see my Scutellaria Baicalensis page for more information). I will test those for a couple of months and see what happens. When I say test, by the way, I don’t mean that I will stop taking curcumin. Too many potential risks involved (increase in IgG count and so on). Curcumin is to me what a security blanket is to the Peanuts’ character Linus.Peekaboo?

Ending on a more personal note. I wish to thank those of you who suggested many wonderful names for our new kitten, who will be joining our merry household on July 10 (more or less). My Mom yesterday suggested Peaches, which I really liked. But last night my husband came up with what I consider to be the best name so far: Peekaboo. We will probably spell it the way it should be pronounced in Italian, that is Pikabu. Our mischievous furry baby loves to play peekaboo, so the name fits perfectly. Is there a cuter kitten in the world? I doubt it! I have no super recent photos, unfortunately; this one was taken about a week ago.

Shakespeare Friday Fun: Eat You, Brutus!

My Dad loves Shakespeare, so when I saw this wonderful list of student essay bloopers from Richard Lederer’s website, I just had to post it as part of my “laughter is good for the immune system” project. πŸ˜‰ I tried to edit the list, but I was able only to take out a sentence or two. Too funny! The entire list can be read on Lederer’s website:

Dad, this is for you!

  • Shakespeare never made much money and is famous only because of his plays and sonics. He lived at Windsor with his merry wives, writing hysterectomies, tragedies, comedies, and errors. I don’t see why he is so popular when his writing skills are so low. He wrote in Islamic pentameter, and you can’t hardly understand what he is saying.
  • In one of Shakespeare’s famous plays, Hamlet rations out his situation by relieving himself in a long soliloquy. A soliloquy is a conversation between one person. Hamlet has an edible complex [ ]. Oedipus and Hamlet really had a lot in common, even if Freud had not yet been invented.
  • In Act Five Hamlet talks to Horatio about a skull that has been thrown up. Act Five comes right after Act Four.
  • After Macbeth becomes the Thane of Candor, King Duncan wires Macbeth that he will be spending the night at his castle. Then Lady Macbeth tries to convince Macbeth to kill King Duncan by attacking his manhood. All Macbeth does is follow his wife’s odors. He kills the king on page 14. Macbeth and Lady Macbeth then suffer from quilt. In fact, they have so much quilt between them, they can’t sleep at night.
  • During the banquet scene, Lady Macbeth is afraid her husband will expose himself in front of his guests. Then Lady Macbeth gets kilt. The proof that the witches in Macbeth were supernatural is that no one could eat what they cooked.
  • Romeo and Juliet are an example of a heroic couplet. Romeo and Juliet belonged to the families of the Montages and Copulates, and Lady Copulate disliked Romeo.
  • Romeo saw Juliet for the first time at the massacred ball. They tell each other how much they are in love in the baloney scene. After much fighting in the pubic square, Romeo’s last wish is to be laid by Juliet. When Juliet died, they had a funeral in her wedding dress.
  • In Julius Caesar, Brutus is a tragic hero despite dying at the end. In Julius Caesar, the toothslayer warned Caesar to beware the March of Dimes. He is murdered by the Ides of March because they think he is ego-testical. Dying, he gasps out the words “Eat you, Brutus!” Then he dies with these immortal words: “Veni, vedi, vici.”
  • In The Merchant of Venice, the Rialto is the business part of Venus. Bassanio loved Portia, but he had no money to press his suit. Taming of the Screw is a play about Petruchio, who takes Kate from a bitter screw to an obedient wife. In A Midsummer Night’s Dream, Puck turns Bottom’s head into an ass. The clown in As You Like It is named Touchdown.
  • In Anthony and Cleopatra, Cleopatra reclined to become Mark Anthony’s mistress. She took the Roman Empire one man at a time. The barge she shat on, like a burnished throne, glowed on the water. The poop was beaten gold.
  • Writing at the same time as Shakespeare was Miguel Cervantes. He wrote Donkey Hote. The next great author was John Milton. Milton wrote Paradise Lost. Then his wife died and he wrote Paradise Regained.

Helicobacter Pylori and MGUS

I have debated whether or not to write a post on this topic. Well, in the end, I decided to give it a go, even though this may turn out to be one of my more controversial posts. I will proceed by degrees. First of all, what is Helicobacter pylori? Medicinenet ( defines it as follows: Helicobacter pylori (H. pylori) is a bacterium that causes chronic inflammation of the inner lining of the stomach (gastritis) in humans. This bacterium also is the most common cause of ulcers worldwide. H. pylori infection is most likely acquired by ingesting contaminated food and water and through person to person contact. I happened to glance at some photos of this bacterium. Nothing cuddly about it, that’s for sure! Yuck.

At any rate, some time ago I came across a study on H. pylori and MGUS conducted at the University of North Dakota School of Medicine and published in The American Journal of Gastroenterology in June of 2002 ( The abstract concludes the following (talk about a shocker!): RESULTS: Sixty-nine patients with MGUS were included in the study. Of these, 57 had undergone evaluation for H. pylori infection for various GI symptoms. Thirty-nine of 57 patients (68.42%) with MGUS also had evidence of H. pylori infection. In 11 of these 39 patients (28.21%), eradication of H. pylori infection with an appropriate regimen led to normalization of the serum protein electrophoresis and resolution of the gammopathy. CONCLUSION: The results of our study give increased credibility to the theory that in a proportion of patients the pathogenesis of MGUS involves chronic antigenic stimulation and H. pylori is implicated. The search for H. pylori infection and an attempt to eradicate the bacterium in positive cases seem to be appropriate in patients diagnosed with MGUS.

Now, before those with MGUS get all excited and start running to the lab to be tested for H. pylori, let me say that a subsequent report by a Mayo Clinic research team, published in the December 2002 issue of the British Journal of Haematology (, contradicts those findings. The Mayo researchers found that there was not a significant difference between a group of MGUS patients (93 people) and a control group (98 people) who tested positive for H. pylori. And, after being treated for the H. pylori infection, those with MGUS still had MGUS.

I read a couple of abstracts about individual patients with H. pylori. A German study ( published in 2006 examined the case of a patient with dyspepsia associated with H. pylori-related erosive gastritis, in addition to Russell Body formation (an inclusion body found in plasma cells) and MGUS: Following H. pylori eradication, gastritis and dyspepsia gradually resolved but MGUS persisted for at least 22 months. Does that mean that the patient’s MGUS disappeared after 22 months? Since I didn’t and don’t have access to the full study, I have no idea. And a 2003 Greek study ( looks at the case of a patient with a long history of chronic gastritis and gastric ulcers with recurrent gastrointestinal hemorrhage who developed a gastric plasmacytoma. The patient took antibiotics to get rid of the H. pylori, and within three months the plasmacytoma had disappeared. The study, which (again) I was unable to access, looks at a possible causal link between the patient’s infection and plasmacytoma.

Okay, so what happens even if you test positive for this nasty bacterium? If you are a curcumin-taker, apparently you don’t have to worry about it too much. Consider the following: a 2002 study shows that curcumin inhibits the growth of H. pylori:; a 2003 German study ( concludes that curcumin, due to inhibition of NF-kappaB activation and cell scattering, should be considered as a potential therapeutic agent effective against pathogenic processes initiated by H. pylori infection.” A more recent Italian study, published in Helicobacter in 2007 (, examined 25 H. pylori-positive patients (twelve men ranging in age from 31 to 76) with functional dyspepsia. The Italian patients were given a dose of curcumin and a few other substances for one week, as follows: curcumin 30 mg b.i.d., bovine lactoferrin 100 mg b.i.d., N-acetylcysteine 600 mg b.i.d., and pantoprazole 20 mg b.i.d. (B.i.d. means twice daily, by the way, from the Latin bis in die). The study concludes: This novel therapy was not effective for H. pylori eradication. However, despite the bacterium persistence, significant improvement of dyspeptic symptoms and reduction of serologic signs of gastric inflammation were observed after 2 months at the end of the 7-day treatment schedule. In my opinion, there are a few weaknesses in this study. The length of treatment–seven days–was too short. From the abstract, in fact, it is not clear (at least to me) if the patients continued with the treatment for two months or if they stopped after the first week. Even if the former were the case, though, 60 mg of curcumin a day is such a small quantity that I am not surprised that the novel therapy didn’t work. For the sake of comparison, I am taking 8,000 mg a day! However, what is rather significant is the fact that even after being treated with such a tiny amount of curcumin (plus the few other substances) these infected patients showed significant improvement in a two-month period. There are other curcumin and H. pylori studies, but these should suffice.

I am not taking sides on this issue. I have read only the abstracts of all these studies, plus I am not a scientist, just a researcher (with a Ph.D. in a non-scientific subject) who happens to have SMM. However, I admit that this Helicobacter business intrigued me enough to bring it up in April with my haematologist. And, in order to leave no stone unturned, I requested to be tested for Helicobacter pylori. At least, I will know if I have it or not. I am beyond MGUS by now, but you never know

Dung on a Twig or Anti-Cancer Treatment?

“Mistel” is the Anglo-Saxon word for “dung,” and “tan” is the word for “twig.” That gives us “mistel-tan, or dung-on-a-twig ” So, still in the dark? πŸ˜‰ Ok, a few more hints. For the Druids, this was a sacred plant, whose name is based on the ancient observation that its seeds would appear on bird droppings (hence, the dung part of its name). It has been around perhaps for millions of years, is a semiparasitic plant that grows on trees, and provides shelter and food for a great variety of insects, birds and animals. Even though it is very toxic to humans, according to the National Cancer Institute FAQ page it has been used for centuries to treat medical conditions such as epilepsy, hypertension, headaches, menopausal symptoms, infertility, arthritis, and rheumatism. Still puzzled?

Ready? Okay, here goes! The mysterious plant is…mistletoe! Yep, the kiss-your-sweetie-under-it-at-Xmas kind of mistletoe! Why mistletoe?

Well, this is what happened. The other day I read about a mistletoe extract, Viscum Album, in a study that a friend (grazie!) sent to me on natural compounds that inhibit angiogenesis. And, as usual, almost grinning, I did an online search. And there it was, quelle surprise!: a mistletoe (extract)-MM study published in a German journal in June of 2006. The abstract can be seen at: An excerpt: None of the three B lymphoma cell lines and none of the three multiple myeloma cell lines produced interleukin (IL)-6 spontaneously or after treatment with VA Qu extract. ( VA Qu, by the way, simply means Viscum Album Quercus.) The mistletoe extract inhibited the proliferation of MM cells, which eventually died. How about that? Another MM-cell killer in vitro.

Funny thing is, before reading this abstract, I had no idea that mistletoe was used as a complementary treatment for some forms of cancer here in Europe Γ’β€šΒ¬”Germany, in particular. A recent (May 2007) International Congress on Complementary Medicine Research held in Munich (the program is available here: featured nine papers on mistletoe presented by eight different researchers. (Not one on curcumin; just thought I would make a note of that πŸ˜‰ ). I then did a Google search in Italian (mistletoe is vischio), too, and a lot of items popped up. Hmmm, very interesting. As I mentioned, mistletoe berries and leaves are toxic to humans (seizures and death are listed among the lovely side effects)–so don’t go chewing on the mistletoe you may have on one of the trees in your back yard–but that is NOT the case for mistletoe extracts, which have few side effects. As reported by the above-mentioned NCI FAQ page (, Mistletoe is used mainly in Europe, where a variety of different extracts are manufactured and marketed as injectable prescription drugs. These extracts are not available commercially in the United States. And, further down, Mistletoe extract is studied as a possible anticancer agent because it has been shown to: Boost the immune system. Kill cancer cells in the laboratory. Protect the DNA in white blood cells, including cells that have been exposed to DNA-damaging chemotherapy drugs.

The NCI page also states that the use of mistletoe as a treatment for cancer has been investigated in more than 30 clinical studies. Reports of improved survival and/or quality of life have been common, but nearly all of the studies had major weaknesses that raise doubts about the reliability of the findings. According to the Dana-Farber Cancer Institute (, among these weaknesses were the small number of patients, inadequate documentation on mistletoe use, etc. However, that said, the U.S. Clinical Trials website currently lists a couple of mistletoe-cancer clinical trials in the U.S. and another one at the University of Heidelberg, Germany.

A February 2007 study ( showed that a mistletoe extract prevented the suppression of natural killer, or NK, cells in colorectal cancer patients undergoing major surgery. A 2004 study ( states that a mistletoe extract called IscadorQu inhibits tumor and endothelial cell growth by delaying cell cycle progression and by causing apoptotic cell death. The antiangiogenic and apoptotic properties of a mistletoe extract are also examined in a 2001 study ( This is turning into a laundry list, so enough.

I would like to end by saying that I am certainly not advocating the use of mistletoe to treat MM. One mistletoe-MM study is not enough to convince my sceptical brain. So, you would probably ask me, why did I even bother to write this post? Well, once I read the origin/meaning of the word, I just couldn’t resist! πŸ™‚ And besides, you never know some day, our view of mistletoe might change, and the use of the following insult–“yeah, well, go poop on a stick!” (found in the online Urban Dictionary, no kidding)–might take on quite another meaning. πŸ™‚

Blood Tests, Zyflamend and Capsaicin Update

Blood. I went to have my blood tests at Careggi hospital this morning. From now on, my friend and I are going to try to have our tests done at the same time, depending on our schedules etc. This morning, chatting about this and that, time simply flew by, and we were out and having breakfast in a nearby café by 8:15 a.m. or so. However, since I had requested that certain minerals (magnesium, etc.) and vitamins (B12, etc.) be checked, I discovered, to my horror, that I won’t have my test results until the end of July-beginning of August! I guess I won’t be holding my breath…

Zyflamend. Talk about coincidences. After reading one of Dr. Benelli’s books on curcumin and other NF-kB and COX-2 inhibitors, I looked up holy basil and read about Zyflamend, which is a blend of various herb extracts. Well, right there and then I decided to order a two-month supply, which my parents (who live in the States) are bringing to me this summer. And here is the coincidental part: just yesterday I came across a recently published study by Prof. Aggarwal and others on this polyherbal mixture: Among other things, Zyflamend was found to inhibit NF-kB, down-regulate COX-2 and suppress osteoclastogenesis. Well, well. I know, I have broken my vow not to post about brands on my blog, but this bit of news was too good to keep to myself. Here is the list of herb extracts contained in this product: Rosemary (leaf), Turmeric (rhizome), Ginger (rhizome), Holy Basil (leaf) extract, Green Tea (leaf) extract, Hu Zhang (Polygonum cuspidatum) (root and rhizome) extract, Chinese Goldthread (root) extract, Oregano (leaf) supercritical extract, Baikal Skullcap (Scutellaria baicalensis) (root) ethanolic extract. This blend comes so close to my idea of putting different anti-MM plant extracts into a bioavailable capsule…

Capsaicin. Ever since reading about capsaicin and MM (see my page on this topic), I have been adding hot red pepper to my food. But I have an exciting update. Prof. Aggarwal, the magnificent Dumbledore of scientific research, recently co-authored a study concerning the effects of capsaicin on the STAT3 pathway in human MM cells. The “Clinical Cancer Research” May 2007 abstract can be read at: I am hoping to access the full study soon. At any rate, here are a few excerpts (practically the entire abstract…!): We found that capsaicin inhibited constitutive activation of STAT3 in multiple myeloma cells. [ ] Capsaicin also inhibited the interleukin-6-induced STAT3 activation. [ ] Capsaicin down-regulated the expression of the STAT3-regulated gene products, such as cyclin D1, Bcl-2, Bcl-xL, survivin, and vascular endothelial growth factor. Finally, capsaicin induced the accumulation of cells in G(1) phase, inhibited proliferation, and induced apoptosis, as indicated by caspase activation. Capsaicin also significantly potentiated the apoptotic effects of Velcade and thalidomide in multiple myeloma cells. When administered i.p., capsaicin inhibited the growth of human multiple myeloma xenograft tumors in male athymic nu/nu mice. It’s almost time for lunch, so pass the capsaicin, please! πŸ˜‰

Random Snippets

This morning, while sipping my usual cappuccino, I watched a trailer from the new Harry Potter movie, which will be in theatres on July 11, and was reminded that the final HP book is about to be published. Oh, no! That will be a very sad day for all of us HP fans, even though I AM looking forward to reading the final chapter of the saga. At any rate, the trailer made me think back to when I mixed curcumin powder with warm coconut milk and pretended to be putting together a health potion in one of Snape’s classes. A bit of this, a bit of that, and poof!, here is the MMCA, or Multiple-Myeloma-Cell-Apoptosis, potion! Now I just swallow capsules, which doesn’t give me the same feeling of power that I had while watching my white coconut milk turn bright orange. Other things that I watched turn orange (permanently, and in blotches) were a couple of my nice white cotton turtlenecks. πŸ˜‰ No matter. At any rate, I have decided to go back to making my powder potion, my elixir of life, next fall.

Random HP thought: for all you HP fans, I don’t think Snape is bad mark my words.

Tomorrow I am going to Careggi hospital (Florence’s main hospital) to have my blood tests done. I have been procrastinating for a couple of reasons: 1. hope that my resveratrol capsules would be delivered before the end of the month so I could at least try to finish my resveratrol experiment and 2. hope that there would be ONE cool morning in June so I wouldn’t melt while walking across the sizzling hospital parking lot. But even HP magic could not have altered these two facts of life. My resveratrol (see below) is still sitting in a post office warehouse in Milan, and Florence is one of the hottest and muggiest cities in Italy. Therefore, no more procrastination. I am going to meet a close friend (with SM) very early tomorrow morning up at Careggi. We can chat up a storm as we wait for our numbers to be called. After our blood tests, we plan to have breakfast together. Perfect.

Resveratrol package update. The lost package has been found. That’s the good news. The bad news is that I won’t have it for another two weeks, at least. Bureaucracy. I am resigned.

I took the weekend off. Did almost no research. Yesterday morning I got stumped on a little thing called p38. I finally gave up and went off to play cards with my hilarious girlfriends. I will resume my research today, though. So many substances left on my list!

Curcumin: the Indian Solid Gold

Solid gold, indeed!!! I just finished reading the most remarkable study by an MD Anderson research team on the wonders of curcumin, published in December 2006. It is titled Curcumin: the Indian Solid Gold, and is available online at: I was going to write a summary, highlighting what I thought were the most interesting and relevant points, but I was so overwhelmed by the study that I was unable to do so (but I may try again soon). For now, I will simply urge those interested to go read it for themselves. You won’t believe your eyes. Just think: the bibliographic references consist of 974 items listed on more than 60 pages. Impressive. It will take me days to go through them. That’s what summer holidays are for, I guess! πŸ˜‰

Progression from SMM to MM

A study published in The New England Journal of Medicine this month (the abstract can be read at: looks at the risk of progression from SMM (or smoldering or inactive or asymptomatic myeloma) to symptomatic MM or amyloidosis. Digression: have you ever had an amyloidosis test? I have, and I must say that I almost prefer a BMB! For me, at least, that test was horrible. But it turned out that I do not have amyloidosis, so that at least is a relief. Back to us.

Mayo Clinic researchers looked at 276 patients diagnosed with SMM, most of whom had the IgG type, between 1970 and 1995. The patients were between the ages of 26 and 90 (median age: 64). Only eight patients, or 3 %, were under the age of 40. 59% of all patients eventually developed MM. I won’t repeat what is available online (i.e., what’s written in the abstract), but give a summary of some of the more interesting points made in the full study, which I was lucky enough to read. First, following the study’s indications, let me define SMM. A diagnosis of smoldering myeloma is based on the presence of a serum monoclonal protein level of 3 grams (or more) per deciliter, or the presence of 10% (or more) malignant cells in the bone marrow, but no symptoms, such as too much calcium in the blood, kidney problems, anemia, bone lesions (these are also known as the four CRAB symptoms), or persistent bacterial infections. In other words, no end-organ damage. SMM, like MGUS, should not be treated.

The study divided the above-mentioned patients into three groups: group 1 had a proportion of bone marrow plasma cells of 10% or more and a serum monoclonal protein level of 3 g per deciliter or more; group 2, 10% or more bone marrow plasma cells and a serum monoclonal protein level of less than 3 g per deciliter; and group 3, less than 10% bone marrow plasma cells and a serum monoclonal protein level of 3 g per deciliter or more. Based on this scheme, I would be in the second group.

Progression to MM was more likely with a higher level of monoclonal protein 5 grams versus 2 grams/dL “at the time of diagnosis. (Interestingly, factors such as gender, haemoglobin, serum albumin level had little to do with progression.) Median time to progression was two years for those in group 1, eight years for group 2, and 19 years for group 3. The cumulative probability of progression at 15 years was 87% for the 106 patients in group 1 (10% plasma cells and 3 g or more of monoclonal protein per deciliter), 70% for the 142 patients in group 2 (10% plasma cells and <3 g of monoclonal protein per deciliter), and 39% for the 27 patients in group 3 (<10% plasma cells and 3 g, or more, of monoclonal protein per deciliter). Time was found to be of the essence: the more time passed after the initial SMM diagnosis, the better (more details can be found in the abstract). This is a big difference between SMM and MGUS, where time is not a factor.

What do I conclude from all of these statistics? First of all, let me say that, while this is a very interesting study, numbers don’t scare me. Not a bit. Besides, all we know about these patients is that they had SMM. That’s it. No information on diet, supplement intake (if any) and so on. Too much perhaps vital information is missing, here. Understandably so, of course, given the long period of time involved, i.e., 26 years. But still…

Secondly, as I suppose is slightly obvious from my blog πŸ˜‰ , I am a devoted curcumin-taker, and curcumin has stopped the progression of my MM right in its tracks. My future IgG trend (plotted by my husband on a graph) is finally a downward one. Yet in January of 2006, I would have been in group 1, based on this study. I am now in group 2. And by the end of the year, who knows? (The eternal optimist, as always!)

Therefore, my advice for those who are still lucky enough not to have active disease: it’s time to act. The wait until the other shoe drops off attitude, which I have seen posted more than once on one of the MM listservs, infuriates me. And if your doctor scoffs at diet or exercise or supplements that have scientific backing (and curcumin is not the only one ), pay no attention. Look up the studies, print them out and take them to your doctor. That’s what I have done and still do. The best patient, or perhaps the most annoying one (depending on your point of view!) is a well-informed one.

Funny Wednesday

Long ago, when sailing ships ruled the waves, a captain and his crew were in danger of being boarded by a pirate ship. As the crew became frantic, the captain bellowed to his First Mate, “Bring me my red shirt!” The First Mate quickly retrieved the captain’s red shirt, which the captain put on. He led the crew to battle the pirate boarding party and, although some casualties occurred among the crew, the pirates were repelled.

Later that day, the lookout screamed that there were two pirate vessels sending boarding parties. The crew cowered in fear, but the captain, calm as ever, bellowed, “Bring me my red shirt!” And once again the battle was on. The captain and his crew repelled both boarding parties; however, this time more casualties occurred.

Weary from the battles, the men sat around on deck that night recounting the day’s occurrences, when an ensign looked up at the captain and asked, “Sir, why did you call for your red shirt before the battle?” The captain calmly explained, “If I am wounded in battle, the red shirt does not show the wound, and thus you men will continue to fight unafraid…” The men sat in silence, marveling at the courage of such a man.

As dawn came the next morning, the lookout screamed that there were pirate ships on their way, ten of them, all with boarding parties. The men became silent and looked to the captain for his usual command. The captain, calm as ever, bellowed, “Bring me my brown pants!”

Olive leaf extract kills myeloma cells!

Here we go again. First it was mint leaves, now it’s olive leaves. Yesterday I was looking up something entirely different when I came across oleanolic acid, which is a triterpenoid (how’s that for a mouthful?) compound extracted from plant sources and food (even seedless raisins, I read). But it is also extracted from olive leaves (olea = olive). Olive leaves? Yes, I read that correctly: the leaves of Olea europaea, the common olive tree. I couldn’t stop reading, since I live in a country, indeed a region, famous for its delicious extra virgin olive oil (rightly so). Plus, my cousin is an extra virgin olive oil taster (yes, just like a sommelier, except she tastes and judges olive oil), and our wonderful extra virgin olive oil is given to us by a friend who owns an olive grove here in Tuscany.

So, just for the heck of it, I googled oleanolic acid and myeloma and, wouldn’t you know it?, there it was: a study on an olive leaf extract and MM cells, co-authored by Dr. Kenneth Anderson and published in "Molecular Cancer Therapeutics" in 2004. The full study can be read at: It is quite technical, but the conclusion is clear: a synthetic version of oleanolic acid, known as CDDO-Im, induced apoptosis in myeloma cells.

I called my husband, who laughed boy, those MM cells get killed by practically anything, don’t they? (Don’t we wish?!!!) But it (almost) seems to be true: any plant extract that I have looked up so far, and that has been tested in vitro against MM cells, appears to have an apoptotic effect on these malignant cells. Hmmm. Anyway, back to us and the oleanolic acid-MM study. In the Introduction, we can read that Chemoresistant MM cells have also been reported to inactivate anticancer drugs more efficiently than chemosensitive MM cells […]. In this regard, increases in the expression of glutathione (GSH) or the activity of GSH-related enzymes in MM cells has been associated with resistance to anticancer drugs […]. Novel treatment approaches that overcome such chemorefractory mechanisms may therefore be effective in the treatment of MM. CCDO-Im reduces the levels of GSH, which leads to the apoptosis of MM cells. The study continues: we analyzed the effects of the CDDO C-28 imidazolide ester (CDDO-Im) on MM cells. CDDO-Im is a potent inducer of apoptosis in MM cell lines and primary MM cells. Potent inducer of apoptosis in MM cells? What??? Hold on a sec, I’ll be right back. I am just going to pop over to ask my neighbour for some olive leaves from his gorgeous olive tree (see photo)! I could juice them! (Just kidding or am I? πŸ˜‰ ) detail of my neighbour's olive tree

Other effects of oleanolic acid. It has anti-inflammatory, hepatoprotective and anti-hyperlipidemic properties, see this 1995 study: It has anti-HIV activity, according to this 1999 study:, and wound-healing potential ( A 1999 study ( tells us that it suppresses the abilities of various inflammatory cytokines, such as IFN-, interleukin-1, and tumor necrosis factor-, to induce de novo formation of the enzymes inducible nitric oxide synthase (iNos) and inducible cyclooxygenase (COX-2) in mouse peritoneal macrophages, rat brain microglia, and human colon fibroblasts. CDDO will also protect rat brain hippocampal neurons from cell death induced by beta-amyloid. A 2003 study suggests that it be used in breast cancer therapy: It also "can provide a cheap and accessible source of additive to conventional treatment of hypertension, complicated by stenocardia and cardiac failure" ( There seems to be no end to its potential. Oh, it also fights the bacteria that cause cavities and gum disease, so make sure you include oleanolic acid-containing raisins in your diet. Oleanolic acid can also be found in medicinal herbs such as ligustrum, forsythia, and swertia, which are used in China to treat hepatitis. I will stop here, but there would be much more.

Last but not least, according to the IMF website (, Johns-Hopkins and Dartmouth are testing oleanolic acid, which is now in the preclinical stage. In fact, this excellent bit of news is hot off the press, see the May 22 issue of the Myeloma Minute:!