Recently Diagnosed or Relapsed? Stop Looking For a Miracle Cure, and Use Evidence-Based Therapies To Enhance Your Treatment and Prolong Your Remission
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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Velcade Builds Bone and kills Myeloma
Velcade builds bone and kills myeloma at the same time. Because 90% of MM patients struggle with “skeletal related events” (SRE) at some point during their MM experience, I consider MM to be both a blood cancer as well as a bone disease.
My MM exhibited itself through bone involvement. Unfortunately, velcade had not yet been invented.
Consider thinking outside the FDA Standard-of-Care box-
Aggressive, high-dose treatment therapy plans advocated by the FDA have certainly increased the average life expectancies of newly-diagnosed myeloma patients. Unfortunately, MM patients relapse repeatedly, reach multi drug resistance and die.
MM is an incurable blood cancer.
Consider a similar yet slightly different approach. Consider a low-dose, low toxicity, bone building approach to managing your MM. Consider low-dose velcade from day one. Consider managing your MM rather than attempting a “potentially curative approach.”
Treatment of Myeloma: Cure vs Control
MM patients diagnosed with no bone involvement at a relatively early stage can consider a proteasome inhibitor (velcade) while undergoing integrative therapies shown to enhance this treatment while reducing its toxicity.
A low dose approach to managing MM may result in:
- a higher quality of life
- a greater quantity of life
- fewer side effects
If you are a newly diagnosed MM patient and are curious about a low-dose therapy plan, email me at David.PeopleBeatingCancer@gmail.com
Thank you,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
The effects of proteasome inhibitors on bone remodeling in multiple myeloma
“Bone disease is a characteristic feature of multiple myeloma, a malignant plasma cell dyscrasia. In patients with multiple myeloma, the normal process of bone remodeling is dysregulated by aberrant bone marrow plasma cells, resulting in increased bone resorption, prevention of new bone formation, and consequent bone destruction.
Clinical studies have reported that treatment with the first-in-class proteasome inhibitor bortezomib reduces bone resorption and increases bone formation and bone mineral density in patients with multiple myeloma. Since the introduction of bortezomib in 2003, several next-generation proteasome inhibitors have also been used clinically, including
- carfilzomib,
- oprozomib,
- ixazomib,
- and delanzomib…
Introduction
Bone disease, defined as the presence of at least 1 osteolytic bone lesion or diffuse osteoporosis with compression fractures, is a characteristic feature of multiple myeloma (MM) [1]. Bone disease occurs in MM because of dysregulated bone remodeling, a process in which MM cells interacting with the bone marrow microenvironment disrupt the normal balance between bone resorption and bone formation [2,3]. This disruption of bone homeostasis results in the prevention of new bone formation and leads to bone destruction [2,3].
As a consequence of altered bone remodeling, up to 90% of patients with MM develop bone lesions that can, in turn, cause a sequelae of skeletal-related events (SREs) such as
The occurrence of SREs has been linked to inferior survival [5,6], reduced quality of life [7], and increased healthcare costs for patients with MM [8,9]…
Treatment with bisphosphonates is the current standard of care for the management of myeloma-related bone disease and is recommended for all patients with MM receiving frontline therapy [9].
Bisphosphonates inhibit osteoclasts and thereby prevent bone resorption [10]. Although bisphosphonates have been shown to reduce the incidence and severity of SREs, improve quality of life, and prolong survival (in the case of zoledronic acid) compared with placebo [9], these agents do not restore bone formation [11].
In addition, bisphosphonates have been associated with renal toxicities and osteonecrosis of the jaw, which may limit their long-term use [2,10]. These drawbacks have spurred investigations into other agents that could simultaneously prevent bone resorption and promote bone formation, while also being safe and tolerable [10,11]…
In contrast to bisphosphonate therapy, proteasome inhibition has been found to simultaneously inhibit bone resorption and promote bone formation [11–13]…
In preclinical models, bortezomib has been shown to have varied and substantial effects on the activities of osteoclasts, osteoblasts, and osteocytes. Studies have found that bortezomib
inhibits the differentiation of osteoclasts [54,55],
decreases the resorption capacity of osteoclasts [54],
reduces the total number of functional osteoclasts [56],
and prevents the death of osteocytes [57].
The preclinical results summarized earlier provided the foundation for clinical studies evaluating the effect of bortezomib on bone remodeling in patients with MM and bone disease. Clinical evidence for the beneficial effects of bortezomib (used a single agent or in combination therapy) on bone remodeling has emerged from the analyses of bio-markers of bone metabolism and from direct measurements of bone characteristics performed in patients with newly diagnosed or relapsed/refractory MM…
Supporting this biomarker evidence, imaging studies and analyses of clinical bone disease events have demonstrated that bortezomib has beneficial effects on bone health in patients with MM. Relative to baseline levels, increased bone mineral density, bone matrix deposition, bone volume, and trabecular thickness in patients with MM have been associated with bortezomib treatment [14,68,77,78]…
Conclusions and future directions
Taken together, the findings reviewed herein suggest that proteasome inhibitors as a class substantially influence bone remodeling in MM. Bortezomib, along with next-generation proteasome inhibitors, modify the bone microenvironment from a catabolic state to an anabolic one [81].
Importantly, there is preliminary evidence that next-generation proteasome inhibitors may have even more potent effects on bone remodeling compared with those associated with the use of bortezomib.
Since the evidence suggests that proteasome inhibitors have substantial and beneficial effects on bone remodeling, targeting proteasome inhibitors to bone may be an advantageous therapeutic strategy [89]. The combination of proteasome inhibitors with immunomodulators (such as structural and functional analogues of thalidomide) has a robust rationale that has been shown prospectively to reduce high dose chemotherapy-associated bone resorption resulting in a low incidence of skeletal related events [89].
In addition, the conjugation of proteasome inhibitors to bisphosphonates and loading protea-some inhibitors into bone-specific nanoparticles are recently proposed methods to achieve bone-targeted delivery of proteasome inhibitors [90,91]. These methods are under active preclinical development and, if successful, may enable an even more effective treatment of myeloma-related bone disease…”