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.
Click the orange button to the right to learn more about what you can start doing today.
I am both a multiple myeloma (MM) survivor and MM cancer coach. I have been researching and writing about multiple myeloma for years. I can honestly say that MM patients and survivors must learn about and employ both conventional (FDA approved) and evidence-based non-conventional therapies if they are to manage their “incurable” blood cancer.
Curcumin is one of the best examples of an evidence-based non-conventional cancer therapy. The applications of this wonder therapy are too many to write about (but scroll down the page to read research citing the anti-MM, pro-kidney, pro-bone health action of curcumin supplementation.
Suffice to say that if you have been diagnosed with cancer, any cancer, you must learn about possible applications of this therapy to help you in the weeks, months and years ahead. In the age of super high tech oncology it is critical to learn about non-toxic therapies such as curcumin.
If you have been diagnosed with multiple myeloma, curcumin has been shown to be cytotoxic (kill) MM itself as well as enhance the efficacy of both Velcade and Revlimid.
Also, according to the study linked below, curcumin promotes kidney and bone health. Kidney and bone damage can be a life-long challenge for multiple myeloma survivors.
I supplement with Life Extension Super Bio Curcumin as this formula and brand are approved both for purity and bioavailability.
Please scroll down the page, post a question or comment and I will reply to you ASAP.
“In the present study, a large panel of human myeloma cell lines (HMCLs) (n = 29), representing the main molecular MM subgroups, was screened for curcumin sensitivity. We observed that curcumin cell death induction was heterogeneous, of note 16 HMCLs were highly sensitive to curcumin and only 7 HMCLs were weakly sensitive.
Cell lines harboring the t(11;14) translocation were less sensitive (median LD50 32.9 μM) than non-t(11;14) (median LD50 17.9 μM), which included poor prognosis t(4;14) and t(14;16) cells.
Interestingly, curcumin sensitivity was not dependent on TP53 status. For the first time we showed that primary myeloma cells were also sensitive, even those displaying del(17p), another poor prognosis factor.
Altogether, these results support clinical trials including curcumin in association with standard therapy.”
“Curcumin, an active ingredient in the traditional herbal remedy and dietary spice turmeric (Curcuma longa), has significant anti-inflammatory properties. Chronic kidney disease (CKD), an inflammatory disease, can lead to end stage renal disease resulting in dialysis and transplant. Furthermore, it is frequently associated with other inflammatory disease such as diabetes and cardiovascular disorders.
Recent studies have shown that increased intestinal permeability results in the leakage of pro-inflammatory molecules (cytokines and lipopolysaccharides) from gut into the circulation in diseases such as CKD, diabetes and atherosclerosis.
This effect of curcumin on intestine can explain why, despite poor bioavailability, curcumin has potential anti-inflammatory effects in vivo and beneficial effects on CKD.”
“Results- Autophagy of rat femoral bone tissue was activated following fracture, increasing with time, reaching a peak at 24 hours. Imaging and histology showed that curcumin promoted the fracture healing in rats, which was reduced by treatment with 3-MA. Immunohistochemistry, immunofluorescence, and Western blot showed that curcumin treatment increased the expression of Beclin-1 and LC3-II, which were reduced by treatment with the autophagy inhibitor, 3-MA.
Conclusions-The findings of this study, in a rat model of femoral bone fracture healing, showed that curcumin promoted bone healing and autophagy, which were reduced by treatment with 3-MA, a known inhibitor of autophagy.”