Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
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Could the ultimate multiple myeloma therapy be a non-toxic, non-conventional supplement? According to the study linked and excerpted below, resveratrol is both:
While there is a long and growing list of FDA approved conventional myeloma chemo regimens, all MMers face the prospect of multi-drug resistance or MDR.
As a long-term multiple myeloma survivor who has undergone high doses of chemo and radiation I have a high risk of secondary cancers as well as a variety of side effects. I’ve been supplementing with resveratrol for years. I take Life Extension Optimized resveratrol because of its unique combination of ingredients. Optimized Resveratrol combines both resveratrol as well as quercetin in one capsule.
According to the studies linked and excerpted below, both resveratrol and quercetin inhibit MM as well as integrate with chemotherapy.
Living with multiple myeloma since my diagnosis in ’94 has taught me that evidence-based, non-toxic therapies such as resveratrol and quercetin are needed therapies for MM patients and survivors. Nutritional, anti-oxidant, anti-angiogenic supplementation coupled with diet, frequent, moderate exercise and other non-toxic therapies make perfect sense for multiple myeloma patients.
Please watch the video below to learn more about the evidence-based, integrative therapies to combat treatment side effects and enhance your chemotherapy.
Resveratrol inhibits proliferation, induces apoptosis, and overcomes chemoresistance through down-regulation of STAT3 and nuclear factor-κB–regulated antiapoptotic and cell survival gene products in human multiple myeloma cells
“Discussion– The aim of this study was to determine whether resveratrol could suppress the proliferation of multiple myeloma (MM) cells by interfering with NF-κB and STAT3 pathways. RES inhibited the proliferation of human multiple myeloma cell lines regardless of whether they were sensitive or resistant to the conventional chemotherapeutic agents.
It also potentiated the apoptotic effects of bortezomib and thalidomide. RES induced sub-G1 accumulation and increased Bax, leading to caspase-3 activation. This correlated with down-regulation of various proliferative and antiapoptotic gene products, including cyclin D1, cIAP-2, XIAP, survivin, Bcl-2, Bcl-xL, Bfl-1/A1, and TRAF2. These effects of resveratrol are mediated through suppression of constitutively active NF-κB through inhibition of IκBα kinase.
Resveratrol also inhibited both the constitutive and the interleukin 6–induced activation of STAT3. We found that RES inhibited the survival of CD138+ plasma cells from patients with MM and potentiated the apoptotic effect of bortezomib and thalidomide, and this correlated with suppression of constitutive activation of both NF-κB and STAT3.
In agreement with previous reports,4,5,33 we found that all MM cell lines expressed constitutively activated NF-κB and that resveratrol suppressed the activation. Although RES has been shown to inhibit inducible NF-κB activation in cell lines of various origins,18 whether RES can also inhibit constitutively activated NF-κB in MM cell lines has not been previously reported. RES inhibits NF-κB through suppression of constitutively active IKK, which is needed for NF-κB activation. We found that inhibition of IKK by RES led to inhibition of phosphorylation of both IκBα and p65; we also found that resveratrol suppressed constitutively active AKT. Both AKT and IKK have been shown to phosphorylate p65.34⇓–36 AKT has been shown to provide survival signals and inhibit apoptosis.28,37″
“Results: Quercetin inhibited proliferation of MM cells by inducing apoptosis and cell cycle arrest in the G0/G1 or G2 phase(quercetin group vs control,p<0.05).Western blot showed that quercetin activated caspase3,caspase9,PARP-1 and increased cytochrome C release. C-myc and cyclinD1 expression were down-regulated and p21 were upregulated.
Quercetin also displays synergistic inhibition effect with dexamethasone in vitro (quercetin with dexamethasone vs quercetin only or dexamethasone only,p<0.05) and western bolt confirmed these results. In vivo,tumor burdern of xenograft mice modeltreated by quercetin was significantly lower than those of control(quercetin group vs control,p<0.05).
Conclusions: Quercetin inhibits proliferation of MM cells by inducing apoptosis and cell cycle arrest in the G0/G1 or G2 phase through downregulating c-myc and cyclinD1 and upregulating p21 .Quercetin also displays synergistic inhibition effect with dexamethasone. Thus, quercetin combination with dexamethasone therapy may be an effective option for MM patients…”