Kevin,
I have used chemotherapy and herbs concurrently in many patients. While I have had a few who have had profound bone marrow suppression, it is always hard to tell if those patients would have experienced that degree of suppression with the chemo alone, because that is certainly something I see as well. Anecdotally it seems, though, that patients who are significantly blood deficient from a TCM standpoint are more likely to develop more profound bone marrow suppression..which makes sense. And your patient does seem to have Blood deficiency based on the points you mentioned. So I would heed Steve's advice in being ready to change to a more supportive formula during chemo as this may be needed because I do find that is sometimes necessary.
It is my experience that the most vehement debate about concurrent chemotherapy and "supplements" centers around Adriamycin. One of the three mechanisms of action is by oxidative damage. The problem (on both sides of the argument) is that we really don't know how much that mechanism plays into the anticancer effectiveness of the drug and it certainly is responsible for some of the side effects...in particular the cardiotoxicity. If the oncologist you are working with is not so open to the concurrent use of herbs, then one compromise you might consider making to foster a relationship is to have the owner stop the herbs 24 hours before Adriamycin therapy and start them again 48 hours later. You are not likely to convince an oncologist who is uncomfortable about the use of herbs with chemo, but you may be able to foster a working relationship that could be mutually rewarding if you are able to work with each other. Seeing is believing.
There was a 2009 study (we oncos love studies!) evaluating the actual impact of herbs on the effectiveness of Adriamycin, because of the concerns which had been raised on this topic. It showed that the concurrent use of herbs allowed equivalent cytotoxicity using 75% less Adriamycin. So the potential, as Steve said, is definitely there and is in the literature. The natural argument this would raise is would that increase toxicity. As I said, anecdotally I have not experienced that to any significant degree and the increased cytotoxicity was via the effects on the NF-kappa-beta pathway not drug metabolism. This is a big topic and the many pathways involved in cancer development and treatment make this a challenging topic to address from a biomedicine standpoint. That is where anecdotes and the long history of clinical use is so important. Okay, I will get off my soap box now.
Anyway, probably TMI. But, if you like that kind of biomedicine info, here is a little blurb about it from something I had written up for a conference. Otherwise stop here!
Erin
Within earlier literature, there exists concern that inhibition of NF-κβ or other antioxidant therapies may reduce the effectiveness of chemotherapeutic agents. In particular, it has been proposed that some of Adriamycin’s cytotoxic activity is through activation of NF-κβ. While there are studies showing that NF-κβ can inhibit the expression of certain anti-apoptotic genes,(65,66) these reports do not examine the overall effects of NF-κβ inhibition of Adriamycin sensitivity and there is little evidence that NF-κβ inhibition actually decreases the effectiveness of chemotherapy. On the contrary, NF-κβ inhibition (using a small molecule inhibitor of IKKβ) was specifically proven in one study to actually enhance the cytotoxicity of Adriamycin chemotherapy. This study evaluated whether Adriamycin-induced inhibition of NF-κβ proved to be pro-apoptotic or anti-apoptotic in osteosarcoma cells. This study showed that the ability of Adriamycin to inhibit expression of anti-apoptotic genes such as Survivin, Bcl-2 and Bcl-xL was through mechanisms other than NF-κβ. Additionally, Adriamycin-induced NF-κβ expression was actually shown to decrease the apoptotic activity of Adriamcyin and NF-κβ inhibition improved apoptotic cell death in Adriamycin-treated osteosarcoma cells. NF-κβ expression was linked with the ability of osteosarcoma cells to resist the cytotoxic effects of Adriamycin. With the combination therapy, equivalent cytotoxicity was able to be achieved using 75% less Adriamycin.(67)