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!