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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Can chemo cause bone loss in myeloma patients and survivors? Yes, according to both the article and video linked below. As myeloma patients already know, their blood cancer, multiple myeloma, c also cause bone loss.
As you probably know, if you have MM, bone health will become a lifelong endeavor for you.
Agents: Dexamethasone, Prednisone
Common regimens:
VRd (Bortezomib + Lenalidomide + Dexamethasone)
CyBorD (Cyclophosphamide + Bortezomib + Dexamethasone)
KRd (Carfilzomib + Lenalidomide + Dexamethasone)
Bone loss mechanism:
Dexamethasone and prednisone are well-known to induce osteoporosis through:
Inhibition of osteoblast activity
Increased osteoclast survival and activity
Reduced calcium absorption
Clinical relevance: This is one of the primary causes of bone loss in MM patients undergoing chemotherapy.
Agents: Thalidomide, Lenalidomide, Pomalidomide
Regimens: Often combined with dexamethasone (e.g., Rd, KRd)
Bone loss mechanism:
IMiDs themselves do not directly cause significant bone loss, but:
Their combination with steroids amplifies risk.
Long-term use can contribute to fatigue and reduced physical activity, indirectly affecting bone health.
Agents: Bortezomib, Carfilzomib, Ixazomib
Regimens: VRd, CyBorD, KRd, etc.
Bone loss mechanism:
Neutral or even protective effect on bone.
Some studies suggest bortezomib may inhibit osteoclasts and promote osteoblast differentiation.
Agents: Melphalan, Cyclophosphamide
Regimens: High-dose melphalan with autologous stem cell transplant; CyBorD
Bone loss mechanism:
Limited direct effect on bone.
Indirect effects due to general marrow suppression, fatigue, or systemic inflammation may contribute.
Agents: Daratumumab, Elotuzumab, Isatuximab
Regimens: Dara-Rd, Dara-VRd, etc.
Bone loss mechanism:
These agents do not directly cause bone loss.
However, used in combination with steroids, which remain the main concern.
Regimens containing corticosteroids (e.g., dexamethasone or prednisone) are the main contributors to bone loss.
Examples include:
VRd (Bortezomib + Lenalidomide + Dexamethasone)
KRd (Carfilzomib + Lenalidomide + Dexamethasone)
Rd (Lenalidomide + Dexamethasone)
CyBorD (Cyclophosphamide + Bortezomib + Dexamethasone)
Email me at David.PeopleBeatingCancer@gmail.com with questions about non-conventional therapies to enhance your bone health.
Good luck,
“Cancer survivors experience many short- and long-term side effects caused by chemotherapy, including low bone mineral density and deterioration of bone microarchitecture. Administration of chemotherapy drugs to disease-free mice causes rapid bone loss. However, whether the bone effects persist throughout life and the mechanisms responsible remain unclear.
One plausible cause of chemotherapy-induced bone loss is cellular senescence. Here, female mice were administered doxorubicin, cyclophosphamide, and docetaxel, a chemotherapy regimen commonly used in breast cancer patients, in combination with two types of drugs that kill senescent cells (senolytics), namely dasatinib + quercetin or piperlongumine.
Mice receiving chemotherapy experienced a rapid decrease in trabecular bone mass, which was detectable two weeks after initiation of treatment and was associated with increased expression of senescence markers. None of the senolytics prevented the effects of chemotherapy on bone mass.
In separate experiments, we examined the skeletal effects of chemotherapy six and twelve months after the cessation of treatment. The deleterious effects of chemotherapy on bone mass remained up to 12 months after cessation of treatment, while no markers of senescence could be detected in bone.
Together, these results suggest that the deleterious effects of this chemotherapy regimen on bone health are not due to the accumulation of senescent cells…
Chemotherapy drugs increase inflammation, DNA damage, and apoptosis27,28. Some chemotherapy regimens also cause cellular senescence—a process in which cells stop dividing and become resistant to apoptosis29,30….
Previous studies have shown that genetic ablation of p16-expressing cells attenuates the loss of bone mass following doxorubicin administration to mice17 implicating cellular senescence as mediator of the bone loss with chemotherapy…
Thus, a pro-apoptotic effect in osteoblastic cells due to DNA damage could potentially explain both the decrease in bone formation and the predominant effect of chemotherapy on trabecular bone.
Future research with mice in which osteoblastic cell apoptosis is inhibited should elucidate the contribution of cell death to the skeletal effects of chemotherapy…”