Monthly Archives: February 2012

MGUS may increase risk of developing infections…

Today I’d like to post the link to a very interesting article published recently in the “Myeloma Beacon”: http://goo.gl/jIhKJ

Here’s my own experience, which I’ve written about on the blog: in 2005 (= the year of my SMM diagnosis; progression from MGUS, diagnosed in 1999) I had chronic, painful yeast infections. This infection business had actually begun a few years before, as I recall (without checking my medical history documents), but in 2005 it definitely got worse…Couldn’t get rid of the blasted things…Took truckloads of antibiotics in many shapes and forms and strengths, to no avail (except more misery). 

The infections disappeared not too long after I began taking curcumin (January of 2006), and they haven’t come back since. I must say, this was an unexpected and most welcome side effect of the wondrous yellow stuff…

Now, I recall reading somewhere that recurrent infections can be a symptom of progression…where was that? Ah yes, here it is. In the International Myeloma Working Group “Criteria” (2003): http://goo.gl/Fq1BS No, that’s not it. I read something more specific…somewhere else…but I don’t have the time to check it out right now.

Ah wait, here’s a possibly relevant study (“Blood,” 2008): Our observation of an association between MM/MGUS and specific prior bacterial or viral infections suggest that these infectious conditions may be a potential trigger for MM/MGUS development or a manifestation of underlying immune disturbances due to undetected MM or late-stage MGUS. Recurrent infections largely of bacterial origin (septicemia, meningitis, and pneumonia) are often part of the natural history of MM. (Full text: http://goo.gl/AnLLy) Ok, not yeast infections, which, however, definitely have a bacterial origin…

This 2008 study seems to counter what we just read in the Beacon article, doesn’t it? I mean, the former states that infections could be possible triggers both for MGUS and MM, the latter that infections did not increase an MGUS patient’s risk of progressing to multiple myeloma. Well, I suppose many things can change in 3-4 years…

So…which is it, eh? Food for thought…

By the way, many thanks to Dr. James R. Berenson for providing the link to the Beacon article (on Facebook)…

The patient’s environment matters…

A week or so ago, a friend sent me this “Atlantic” article, published in its July/August 2011 issue: http://goo.gl/jd1ow I found it absolutely fascinating, even though I can’t help but disagree with some parts of it (you can imagine which…). I just hope that some day those who vehemently and, in my opinion, blindly oppose any sort of “alternative” approach will learn to soften their unyielding positions and become more open-minded…like Dr. Gertz, a Mayo Clinic hematologist (see page 3)…

Lots of food for thought in this article. Here are a few of my random favorites:

  • YOU MIGHT THINK the weight of the clinical evidence would close the case on alternative medicine, at least in the eyes of mainstream physicians and scientists who aren’t in a position to make a buck on it.
  • In many cases, the drugs used to treat the most-serious cancers add mere months to patients’ lives, often at significant cost to quality of life.
  • THE MEDICAL COMMUNITY knows perfectly well what sort of patient-care model would work better against complex diseases than the infectious-disease-inspired approach we’ve inherited. That would be one that doesn’t wait for diseases to take firm hold and then vainly try to manage them with drugs, but that rather focuses on lowering the risk that these diseases will take hold in the first place. “We need to prevent and slow the onset of these diseases,” says Blackburn. “And we know there are ways to do that.” Aside from getting people to stop smoking, the three most effective ways, according to almost any doctor you’d care to speak with, are the promotion of a healthy diet, encouragement of more exercise, and measures to reduce stress. [Blackburn = Elizabeth Blackburn, a biologist at the University of California at San Francisco and a Nobel laureate. ]
  • Studies by her and others have shown that stress is linked to the shortening of telomeres, and shorter telomeres are in turn linked to aging and cancer. “We tend to forget how powerful an organ the brain is in our biology,” Blackburn told me. “It’s the big controller. We’re seeing that the brain pokes its nose into a lot of the processes involved in these chronic diseases. It’s not that you can wish these diseases away, but it seems we can prevent and slow their onset with stress management.” Numerous studies have found that stress impairs the immune system, and a recent study found that relieving stress even seems to be linked to slowing the progression of cancer in some patients.
  • Numerous studies have found that stress impairs the immune system, and a recent study found that relieving stress even seems to be linked to slowing the progression of cancer in some patients.
  • Hippocrates put it this way: “It is more important to know what sort of person has a disease than to know what sort of disease a person has.”
  • Many medical students start out with a healer mentality, but few retain it. “It gets beaten out of you by the system,” says Brian Berman, noting a study showing that medical students score progressively lower on empathy tests the further they get into their training. Berman himself was a conventional M.D. until, at age 33, he took up the study of traditional Chinese medicine—which, like many alternative approaches, is largely focused on patients’ lifestyles, feelings, and attitudes, and which emphasizes stress reduction, healthier eating, and regular exercise, as well as encouraging the patient to believe in self-healing. “I saw how much more I could do to help people,” he says. “For the first time since medical school, I felt like a healer again.”
  • randomized trials have by and large failed to show that alternative treatments work better than placebos.
  • To be approved by the FDA, a drug has to do better than a placebo in studies—but most approved drugs do only a little better, and for many drugs the evidence is mixed.
  • “The randomized trial is a very high bar,” he says. “Eighty percent of what I do here isn’t based on randomized-trial data.” [“he” = Dr. Morie Gertz, Mayo Clinic]
  • The beneficial effects of alternative therapies on Mayo Clinic patients, he says, have been observable in shorter hospital stays, in lower levels of self-administered painkillers, and in reduced tissue inflammation, which is a general indicator that the immune system is better holding its own. [“he” = Keith Lindor, a liver specialist & also dean of the Mayo Clinic’s medical school.]

Okay, I’d like to end with a personal experience, which is (sort of) relevant. Last week my yukky cough returned. Ugh. No wonder, since I’ve been exposed to chronic germ factories all winter = my students, who cough and sneeze almost non-stop (and sometimes even come to work with a high fever, hellooooo!!!). In fact, given my almost non-existent immune system, I’m really surprised that I haven’t gotten the flu (yet!). Could that be because of my Nigella sativa intake? No idea. Anyway, back to the point: THE COUGH. It soon blossomed into what I normally judge as “a cough that needs antibiotics”: yellow phlegm and a low-grade fever.

But I decided instead to try Manuka honey with a high MGO. I mean, I felt okay, and this occasional cough, similar to what I had last fall but not as violent, didn’t stop me from being active. So I figured, “oh why not? I’ll try it…and keep a close eye on my symptoms.” After a few days, what I was coughing up wasn’t yellow anymore. No kidding. Even I was impressed. Now, I’m not suggesting that this honey will work for everyone. Last year, in fact, it didn’t work for me (although I should mention that I ran out of the high MGO honey and had to take a low MGO one). Boyohboy, though, it would be amazing if I could avoid taking antibiotics…at least on occasion!

And so my question of the day is: do I need to see the results of a randomized controlled clinical trial before taking Manuka honey as soon as I feel a cough coming on?

I think you know my answer…

The Australian MGUS and SMM-curcumin trial data just got published…(Part 2)

Yesterday morning I received a Google Alert about this important trial. A few blog readers also “alerted” me to its existence (thanx!). I tracked down and devoured the full study. As mentioned in yesterday’s post, you can read the abstract here: goo.gl/bcVxt

Let’s see. Based on the abstract, curcumin had a strong positive effect on the free light chain ratio…It also decreased a marker of bone resorption called uDPYD (= “urinary deoxypyridinoline”; without too much ado, let me just say that keeping it down down down is a good thing!) and diminished creatinine levels. Take my word for it: all good stuff!

Quick personal note: my own FLC ratio fluctuates madly with each test, down and up and down again, but I just read a sort of “P.S.” on my report, stating that this test doesn’t distinguish between polyclonal and monoclonal free light chains. Hmmm, not sure what to make of that… Another problem: I didn’t have my FLCs tested in the pre-curcumin period. Back then, I didn’t even know about ’em, let alone that they could be tested. So I can’t do any comparative work, since I don’t know what my baseline was…Too bad. However, on the Binding Site, I still turn out to be MGUS with BM suppression. So I’m not going to worry my pretty little head over thaaaat! 😉

Let’s get to the abstract conclusions: These findings suggest that curcumin might have the potential to slow the disease process in patients with MGUS and SMM.

I tell ya, after years of watching doctors roll their eyes at me and tell me that there was no way I could slow down the progress of this terrible cancer, I feel vindicated. Finally and completely. I mean, I’ve felt vindicated on a few occasions in the past few years, too. But this time it’s different…The results of this Australian trial, in which MGUS and SMM folks participated, have really put a lovely, delicious cherry on my (chocolate, of course!) cake. What I read yesterday confirms, to me anyway, that I made the right choice when, more than six years ago, I decided to take the “alternative” fork in the myeloma road…Not an easy choice, mind you. No, not back then. But I don’t want to dwell on the past…not today!

Okay, now, without revealing too many details (I don’t want to get into any trouble!), let me dive into the full study.

Its aim was to find out if a dose of 4 or 8 grams would have any effect on MGUS and SMM.

Now this is interesting. The patients in the curcumin “arm” swallowed (with yoghurt or another fat) C3 curcuminoid granule stick-packs. Stick-packs? Never heard of those. Of course, those who got a placebo for the first three months also swallowed stick-packs, without the curcumin inside ‘em, of course. Quick but important note: the study declares all the placebo ingredients, by the way, which is REALLY GOOD…Do you remember my recent placebo post? Yikes!

The main markers tested were: paraprotein, FLC values, total protein, B2M, PTH, albumin and creatinine. The one that stood out to me was the PTH test. PTH stands for parathyroid hormone. I mean, why was PTH preferred to, say, serum calcium, uric acid or LDH? Hmmm…perplexing. However, it turns out that a few patients had hyperparathyroidism, which is what I suffer from on occasion, when my vitamin D levels drop too much (I try to be careful about that!). Coincidence? Oh…bloody ‘ell, I have no idea what that means…I might have to write to the main author about this…Ok, let’s keep going…

I was super curious to find out what happened to the patients that dropped out of, or were excluded from, the study. What happened is that a few didn’t follow the program correctly, and a few progressed to active myeloma (based on which parameters, I wonder…hmmm…I’d love to know that…) and began doing chemotherapy. Incidentally, in “group A” (the original curcumin arm, that is), two of the four SMM patients who began chemo chose to continue taking curcumin. Three cheers for them! I’d love to know how they’re all doing…Does anyone know? (If you read my blog, please get in touch with me…I’d be thrilled! Thanks.)

As for group B, the original “placebo” arm, two patients left the study because of diarrhea issues, and one SMM patient progressed to full-blown myeloma.

Their data was therefore excluded.

Okay, let’s see what else we’ve got. No big changes occurred in paraprotein at the 4 gram dose. The big changes were the FLC ratio and the bone resorption marker, which, ahaaaa!, increased (= not good, eh) when the patients switched over to the placebo. That’s significant, I’d say!

Now we’re going to leave the 4 gram/day study and have a look at the subsequent, 8 gram/day curcumin arm. Here we have a total of 18 patients (9 from each group) who experienced significant reductions in FLC values, total protein and random urinary protein, as well as in uDPYD and PTH. Yaaaay! No changes noticed in serum albumin, B2M or hemoglobin.

I wanted to check those last three results against my own tests, but I ended up in a bit of a quagmire. The one that’s absolutely certain is hemoglobin. My Hb hasn’t changed a smidgen since the pre-curcumin period, when it was 13.2. It’s still 13.2. So, while curcumin is a metal chelator, at least it hasn’t made me anemic! What it did do, thank goodness!, was bring down my dangerously-near-the-high-end-of-the-normal-range iron levels to more manageable levels (my serum iron is now 72 micrograms/dL, as opposed to being in the upper hundreds. In one 2005 test, it even went to 164 mcg/dL, that is, 24 points above the reference range, yikes). And, since it’s not good to have high iron levels, I’m really happy about that. As for B2M and albumin, I was sorry to notice that their reference ranges have really changed over the years (verrrry annoying!), so it’s impossible to tell… Uff!

Oh well. Back to Australia, now. Remember, we’re having a look at the 8 gram takers, now. Here’s a good one: patients who began the study with an abnormal FLC (most of ‘em, that is) also had a reduction in their paraprotein levels, and this is important, since apparently this didn’t occur at the lower, 4 gram dose.

This seems to confirm that 4 grams is not a high enough dose if we really want to have an impact on our numbers. Just my interpretation, of course…

I know I shouldn’t be quoting from the full study, but I hope it’s okay to share this with you: To our knowledge, this is the first randomised study to show a beneficial effect of curcumin on light chains in MGUS and SMM patients. Normalization of the FLC ratio has previously been shown in myeloma patients after chemotherapy and have been reported to be highly predictive of achieving a complete response. Complete response, huh? Sweet. 

The study ends on an important note: None of the 25 patients who completed the 4g study (which includes the 18 on 8g/day) have progressed to active disease one year after the study has been completed. (Oh drat…another quote…ehm…)

Of course, only time will tell. But all these positive findings, all the improvements in important markers confirm that, for some of us (= those of us taking a higher dose, those of us who have wacky FLC numbers and so on…), perhaps most of us!, curcumin can indeed be a powerful helper in the battle against this terrible cancer. I’m living proof of that, aren’t I?

For now, anyway… 😉

Thank you, Australia!!!

The Australian MGUS and SMM-curcumin trial data just got published…

That’s right. I just finished reading the just-published Australian MGUS and SMM-curcumin trial results. All the new data. Wow. Here is the abstract: http://goo.gl/bcVxt This, incidentally, was a randomised, double-blind placebo-controlled cross-over study, followed by an open-label extension study… whoa…mouthful…

After getting home from work and getting my hands on the full text (thank you, you-know-who!!!), I wrote a post about it, but I confess to feeling quite tired now. Yeah. Zzzz. Almost time for supper over here in Firenze, Italia. So I’m going to put my draft aside and edit it tomorrow with a fresh mind…Plus, that will give me enough time to go through the study once more to see if I missed any important bits. 

Oh wait, one thing. Please notice the abstract’s Conclusion: These findings suggest that curcumin might have the potential to slow the disease process in patients with MGUS and SMM

POSSIBLY SLOW THE DISEASE PROCESS!!! (I’ll discuss the implications tomorrow.)

Hah and double HAH! So much for what all those multiple myeloma specialists told me in 2005: that there was “nothing” I could do to slow down the progression to active myeloma…So much for that…yup…

Since Stefano isn’t home from work yet, I’m hugging and kissing my youngest kitty, Pinga, who is sitting on her folded cat blanket, between me and the keyboard (her favorite spot). She doesn’t seem all that impressed, though… 😉

CURCUMIN FOREVER!!!

What does curcumin have to do with transgenic fruit flies?

Last week I received a Google Alert that led me to this Science Daily article: http://goo.gl/G1M4b Excerpt: Five groups of diseased flies with different genetic manipulations were administered curcumin. They lived up to 75 % longer and maintained their mobility longer than the sick flies that did not receive the substance. The “disease” in question was an Alzheimer-like one, incidentally.

Well, I’m not a transgenic fruit fly, but even I can tell that I remember things now that I couldn’t possibly have remembered in the pre-curcumin period. And my mind is really sharp. Not that it wasn’t sharp before I started taking curcumin (hate to brag, of course… 😉 ), but now it could be used to cut sheets of stainless steel…Uhm, oh well, er, the fact that I “lost” my myeloma buddy, Honey, for about 36 hours doesn’t count. I mean, I found her again, didn’t I? 😉 (Some time ago, I must have tucked her inside one of the china cabinet drawers to keep her safe from my cats and then had simply neglected to put her back in her usual place. That’s all. Nothing to do with memory…or lack thereof…yeah, that’s it…)

Okayokayokay, quick change of subject! ;), I also wanted to post the link to an adorable video that I watched recently…nothing to do with myeloma, although some of you will recognize the place, which has a lot to do with myeloma: http://goo.gl/xEQsh Awwwww, sweet! The video reminded me of my parents who have been happily married for more than 57 years, still walk around hand in hand and are very active…(they also take about 4 grams of curcumin every day…)

Last but not least, here is another interesting link. Again, a Science Daily article, published last month, about the effect that diet can have on C-reactive protein: http://goo.gl/ixjzU In a few words, a group of healthy people on a low glycemic diet managed to reduce their C-reactive protein levels by about 22%. Twenty-two percent! Wow. That could be really important news for us, since CRP is one of the most important myeloma markers…There is a list of “low glycemic” foods at the end of the article.

Check it out! 

An amazing ashwagandha story and…SURPRISE!!!

Yesterday a blog reader with Non-Hodgkin’s lymphoma left a comment on my Ashwagandha page (see: http://goo.gl/UAsns). Amazing story. And there is more…Check out this New Zealand article detailing his experience: http://goo.gl/48Lm9 Verrrrry interesting, eh? 

Completely off topic, now: I organized a surprise party for Stefano last night. He changed jobs last summer, thank gooooooodness!, and I wanted to celebrate the fact that his six-month trial period was over and he’d been hired on a permanent basis, yaaaay, which is this economy is no small feat… (Of course, I had no doubt that he’d be hired forever, since he’s so incredibly brilliant! :) )

Knowing that I’d be preparing, and filling the fridge with, copious amounts of food in the days preceding the party (food that we wouldn’t be eating, of course!), I’d told the brilliant guy a half-truth so that he wouldn’t suspect anything–that I’d invited my card-playing buddies over for dinner and a card game. Totally plausible. I simply omitted to mention that I’d invited a bunch of our dearest friends as well… :)

The timing was purrfect. Stefano got home from work early, before everyone showed up with more food (and wine), and went straight up to his super computer room. His stereo was on, and he was so engrossed in his work that he didn’t hear or pay attention to how many times the doorbell rang. Luckily.

Once everyone had arrived, I yelled up to tell him that dinner was ready. He came down, expecting to find only the four of us, the mad card players, but there we all were, shouting “SORPRESAAAAA!!!!” He was totally shocked. He stood in the middle of the living room, surrounded by our laughing friends, unable to move, absolutely speechless. They all went over and hugged him, and he finally came out of his reverie…

Well, the party ended up being a huuuuuge success. We talked and laughed and ate and drank and made merry until the early hours of the morning…(In this photo you can see my made-from-scratch cream of pumpkin soup, which was a big hit…and yes, I added some turmeric and Nigella sativa to it, too…) 

But I have to admit that today…today I’m so tired that I barely know my own name… 😉 Tired, but happy, too…

Thymoquinone (from black cumin) kills multiple myeloma cells…

Since it’s possible (only “possible,” eh!) that my recent good results might have been influenced at least in part by my recently increased intake of Nigella sativa, more familiarly known as black cumin, I thought I would discuss two black cumin studies published in the fall of 2011. By the way, black cumin is not the same as regular “cumin.” 

Well, I just had a brilliant idea. Instead of talking about these seeds in an abstract way, why not take a photo of some of my own (organic) seeds for our “Weird seeds 101” lesson? 😉 Okay, here you can see the black cumin seeds on top; cumin seeds, bottom left, and fenugreek seeds, bottom right. For size comparison, I put a pumpkin seed on the top right-hand side…

For the record: after taking this photo, I poured all the seeds back into their separate containers, but I popped the fenugreek ones into my mouth…and yes, I can confirm that they still taste like burnt celery and are as hard as rocks (so it’s better if you cook them…)!

Before I go on, I should also point out that both the 2011 studies CONFIRM the findings of a 2010 study on thymoquinone and myeloma, which I had discussed in this April 2011 post: http://goo.gl/zL0te Different research teams, eh. 

Okay, back to us, finally. The first on my list is a September 2011 study. I’d meant to report about it ages ago, but…things happen, as you know by now (!)…Studies pile up on my desktop, then get stuck in folders and almost forgotten, sigh (I need a full-time assistant! 😉 ). The full text is available for free online: http://goo.gl/9zfwh

The study’s title is daunting, to say the least. But it’s not that complicated, once we know what everything means. For example:

  • CXCL12 is a powerful chemokine (= a cytokine that activates white blood cells during an acute/chronic inflammation), which “lives” in the bone marrow. CXCL12 is one of the super bad guys, mind you, since it fuels both bone destruction AND angiogenesis…aaagh! Oh, as if that weren’t enough, it also activates myeloma cells in the bone marrow…double aaagh! 
  • Chemotaxis are not special taxis that take cancer patients to their chemotherapy appointments (sorry, couldn’t help that one…). Seriously now, it means: “movement toward or away from a chemical stimulus.” Luckily, the study itself provides more details (see the “Discussion” part): chemotaxis is important and critical for the homing, interaction with the BM microenvironment and survival of MM cells. No comment necessary, methinks! But those of you, brave souls!, who would like to read more about chemotaxis and what it means in myeloma can have a look at this 2010 study: http://goo.gl/MIynz
  • Fas-mediated apoptosis: basically, Fas is an apoptosis-signaling receptor molecule. Okay, try this: when cancer cells become resistant to treatment, they thumb their noses at our friend, Mr. Fas, and survive. So we like Mr. Fas. And we don’t want Mr. Fas to be blocked!
  • Thymoquinone, or TQ, is the active ingredient in black cumin oil extract. Like curcumin is the active ingredient in turmeric. And so on.

Okay, now that that’s clear (?), we can proceed…

When myeloma cells were pre-treated with the black cumin extract (= thymoquinone), CXCL12 and CD45 (another evil guy, in the myeloma patient’s guidebook…) weren’t able to communicate with each other. Even if we don’t understand what exactly happened there, take my word for it: it’s good news for us. 

And another good thing: thymoquinone had a strong effect on myeloma cells but not on healthy PBMCs (= peripheral blood mononuclear cells, or immune system blood cells such as lymphocytes) from healthy folks. That means that it attacked only the bad guys…good to know!

Oh, so many details. For example, the fact that myeloma cells treated with TQ have more CD95 on their surface. And CD95 = death of the myeloma cell, via Fas-mediated apoptosis. Oh, and the death of TQ-treated myeloma cells was increased by up to 85%. Fantastique!!!

Conclusions: the present data expand our knowledge of TQ mechanism of action and suggest that TQ may represent a promising drug candidate for the treatment of patients with MM, providing a rationale for its clinical evaluation. Yesssss!

And now for the second study, published in December 2011 (again, full text available for free online): http://goo.gl/c8mtj Note: a couple of the authors are the same as those who worked on the first study. 

The main difference between the two studies is that this one talks specifically about STAT3, which is a hyperactive transcription factor linked to heaps of bad stuff in myeloma. As we know by now, STAT3 is associated with inflammation and the survival, proliferation, metastasis, angiogenesis, and chemoresistance of tumor cells. Blablabla…

Thanks to the 2010 study on the same topic, I was not surprised to read that TQ inhibits the IL-6-induced proliferation of MM cells AND suppresses STAT3 phosphorylation and the expression of its downstream signaling effectors Bcl-2 and Bcl-XL. By inhibiting STAT3, TQ also had a strong effect on many other bad guys in myeloma, such as cyclin D1, the Bcl family, survivin, Mcl-1 and VEGF. Just what we saw happen recently with guggulsterone, incidentally…

Conclusions of study no. 2: Taken together, our data suggests that TQ could potentially be applied toward the treatment of MM and other malignancies. Yes indeedie!

I’m now throwing black cumin seeds into everything we eat, except for our morning cappuccinos 😉 And, when he cooks (he’s a much better cook than I am), Stefano uses it, too…Besides being good for us in more ways than expected (or so I hope, at least!), it also adds a lovely peppery flavour to our food…Give it a try! 

Canadian government plans to poison wolves for the oil companies’ toxic tar sands project

Today I would like to urge you to read this “Huffington Post” article on an absolutely appalling event that is, apparently, about to take place in Canada (Alberta): http://goo.gl/IJ4vd 

If you are a U.S. citizen and agree with me that this is outrageous and should be stopped, then please sign the following petitions: 

1. To the Canadian Prime Minister and the Minister of the Environment: http://goo.gl/BiRhm

2. To our representatives in Congress and the Senate: http://goo.gl/JQUEh

And it’s not just about wolves and the caribou. It’s about protecting a vital habitat for other important species, too (see above article). It’s about protecting our future and that of future generations…

Let’s stop the greedy oil companies before it’s too late…SIGN SIGN SIGN! 

Thank you!

An unexpected delivery…

Yesterday I received a big, soft package from a friend in the UK. I couldn’t believe my eyes when I opened it: she’d knitted me an entire blanket! I was and am soooooo overwhelmed (thank you thank you thank you!). 

It’s so beautiful that I really think I should put it behind glass and hang it on a wall. Well, I do have another reason for saying that: you see, I immediately laid it out on the bed to admire it, but within a minute or so my cats decided it was the best thing since canned tuna. So for now I’ve put it safely away…but only for now. I’ll figure out something…

I did let the kitties have the plastic bag in which it came. That was a huge success, too. Pinga was the first to make her way inside it…and from her safe plastic fort she happily launched many surprise attacks on the other cats passing by. In this photo, she and Peekaboo are resting from a prolonged, back and forth, noisy batbatwhackwhackslamwhackslambatsmack!!! session (incidentally, that fluorescent green thingy is a cat toy).

At one point my totally unaware male cat walked into the room and ambled over to check out and sniff the bulky bag. And boyohboy did he get the surprise of his life, when Pinga lunged at him from her hiding place, smacking him right in the face then darting back inside the bag! He must have jumped three feet in the air…BACKWARD, too! 

I just had to laugh. That Pinga cat…

What’s in a placebo? Surprise, surprise…

Placebos? In my wildest dreams, I never thought I’d write even a tenth of a post about placebos…I mean, what do I care about those “innocuous” sugar pills that cause no side effects? 

But then yesterday I read a recently-published, interesting “Science Daily” article on how placebos can reduce pain: http://goo.gl/OrVGq And, for some obscure reason, it started me wondering…what exactly is inside a placebo?

And so my Google search began…

One of my first hits was an October 2010 paper published in the “Annals of Internal Medicine” and titled: “What’s in Placebos: Who Knows?”: http://goo.gl/ONkdz

Aha. Bingo. 

The first sentence of the abstract tells us that No regulations govern placebo composition. Saywhatwhatwhat??? No FDA standards? Not even the  itsiest bitsiest precept stuck way in the back of a forgotten set of FDA guidelines? Nope. Nothing. 

That’s what the paper’s main author, Dr. Beatrice Golomb, states (see this 2010 “Science Daily” report): http://goo.gl/n6e2p): “…there isn’t anything actually known to be physiologically inert. On top of that, there are no regulations about what goes into placebos, and what is in them is often determined by the makers of the drug being studied, who have a vested interest in the outcome. And there has been no expectation that placebos’ composition be disclosed. At least then readers of the study might make up their own mind about whether the ingredients in the placebo might affect the interpretation of the study.”

Why do I find this disturbing? I mean, I’ve read some really gross stuff about what drug companies do in order to achieve their goals…trial data manipulation and so on… 

And that leads us right to a thorny issue: how can we really trust the results of studies and trials that don’t even disclose what’s in their placebos? I have to admit, if I’d never come across the 2010 Golomb study, I wouldn’t have thought it a relevant issue…but now…hmmm. 

Let’s see. First point: placebos have to LOOK A LOT LIKE (even the way they smell and feel, apparently) the drug being tested in the “controlled” clinical trial. Second point…a much more important one!: the drug companies are making their own placebos. And here let me think out loud: doesn’t it make sense that the drug companies would at least be tempted to use special, uhm, fillers or whatnotsies that might make their drug look better and seem more effective than it really is…? It’s certainly a possibility…

Dr. Golomb and her team found that only 8.2% of placebo-controlled clinical trials revealed what exactly was inside the placebo. They also found that earlier trials of cancer and HIV treatments used placebo pills composed of lactose sugar and found relatively few gastrointestinal problems in the experimental group: AIDS and cancer patients can be at an increased risk for lactose intolerance (from: http://goo.gl/esIf2). In this case, the placebo probably made the experimental drug look better…Of course, the opposite might also occur…

Dr. Golomb adds: “We can only hope that this hasn’t seriously systematically affected medical treatment,” noted Golomb. But she and her team suggest that it is a very real possibility, with potentially serious consequences. “An ineffective treatment might appear effective, or an effective treatment might appear ineffective in trials,” senior researcher Jeremy Howick of the University of Oxford, in England, told Reuters Health in an email. “This is obviously harmful for public health since it could lead to use and payment for ineffective treatments, or failure to recognize effective ones.

Yesterday one thing led to another, and I also read about “active” placebos: http://goo.gl/UyL3y Active placebos? Wait a sec, aren’t placebos supposed to be INACTIVE? Well, no, not really. Active placebos are designed to give patients a few minor (?) side effects similar to those caused by the actual experimental drug. That way, they are fooled into thinking they’re receiving the real deal, not an “innocuous” substitute. Patients in studies and trials talk to one another, you see, which means that those who don’t suffer from any side effects whatsoever would probably get suspicious.

Food for thought. I mean, there might be more to the old “placebo effect” than we thought…

Well, whatever…One thing is for sure: I’m all in favor of DISCLOSURE! DISCLOSURE! DISCLOSURE!!! I mean, tell us what’s really inside those “sugar” or “starch” pills! If I were in a trial, I’d certainly want to know…