Learn how you can stall the development of full-blown Multiple Myeloma with evidence-based nutritional and supplementation therapies.
Click the orange button to the right to learn more.
A diagnosis of monoclonal gammopathy of undetermined significance (MGUS) is a double-edged sword. The good news is that you have caught a possible future incurable blood cancer early and may able to prevent your MGUS from becoming full-blown Multiple Myeloma for years if not for the rest of your life.
The bad news is that you will now spend the rest of your life worrying about your pre-Multiple Myeloma.
Your other challenge with a diagnosis of any form of pre-myeloma (SBP, MGUS, SMM) is that your oncologist will likely tell you that MGUS is asymptomatic and that your only option is to watch and wait.
Research indicates that MGUS patients can reduce their risk of full MM through
Conventional oncology considers all pre-MM states- SBP, MGUS and SMM to be “blood disorders” and therefore offers no therapies to manage them other than a clinical trail or watch and wait.
When I was diagnosed with a form or pre-MM (a single bone plasmacytoma) my oncologist told me that nothing could be done. Yes, there was a small chance (3%) that my SBP would not become full MM but all I could do was to watch and wait.
I am both a MM survivor and MM cancer coach. My experience and research have shown me that MGUS can be managed with evidence-based non-conventional therapies. I have worked with MGUS survivors who have been managing their pre-cancer for 15 years or more.
To learn more about the evidence-based protocols you can follow to prevent your Pre-Myeloma from becoming Multiple Myeloma, ask me a question or write a comment below.
Monoclonal gammopathy of undetermined significance (MGUS) is a clinically asymptomatic premalignant clonal plasma cell or lymphoplasmacytic proliferative disorder. It is defined by the presence of a serum monoclonal protein (M protein) at a concentration <3 g/dL, a bone marrow with <10 percent monoclonal plasma cells, and absence of end-organ damage (lytic bone lesions, anemia, hypercalcemia, renal insufficiency, hyperviscosity) related to the proliferative process.MGUS occurs in over 3 percent of the White population over the age of 50 and is typically detected as an incidental finding when patients undergo a protein electrophoresis as part of an evaluation for a wide variety of clinical symptoms and disorders (eg, peripheral neuropathy, vasculitis, hemolytic anemia, skin rashes, hypercalcemia, or elevated erythrocyte sedimentation rate).
There are three distinct clinical types of MGUS, each with a risk of progressing through a unique intermediate (more advanced) premalignant stage and then to a malignant plasma cell dyscrasia or lymphoproliferative disorder :
●Non-IgM MGUS (IgG, IgA, or IgD MGUS) – Non-IgM MGUS is the most common subtype of MGUS and has the potential to progress to smoldering (asymptomatic) multiple myeloma and to symptomatic multiple myeloma. Less frequently, these patients progress to AL amyloidosis, light chain deposition disease, or another lymphoproliferative disorder.
●IgM MGUS – IgM MGUS accounts for approximately 15 percent of MGUS cases. It is considered separately from the non-IgM MGUS because it has the potential to progress to smoldering Waldenström macroglobulinemia and to symptomatic Waldenström macroglobulinemia, and less often to lymphoma or AL amyloidosis. Infrequently, IgM MGUS can progress to IgM multiple myeloma.
Dr. Stephen Cohen–Have you ever wanted to read the notes and observations of a practicing compassionate and empathetic doctor who has cared for cancer patients for over 40 years? Well, now you can! Dr. Stephen Cohen, a medical oncologist and hematologist practicing in San Antonio, Texas, has kept a daily journal of interesting medical info and tidbits he encounters day to day from his personal experiences with patient care, professional journals he reads, and medically relevant information on all subjects that he comes across.
Multiple Myeloma evolves from a monoclonal gammopathy of undetermined significance (MGUS).
Only 10% of patients with newly diagnosed myeloma have a history of pre-existing MGUS.
MGUS almost always precedes myeloma.
Smoldering myeloma is an intermediate stage between MGUS and myeloma is associated with a higher risk of progression of approximately 10% year.
MGUS arises from a premalignant proliferation of monoclonal plasma cells derived from post-germinal B cells, that undergo genetic and microenvironmental changes leading to the transformation of these cells into a malignant process.
MGUS is a disorder of the terminally differentiated B lymphocytes, called plasma cells.
Plasma cells secrete monoclonal immunoglobulin, IgG in about 60%, IgA in about 20%, for light chains in 20%, IgD in 2%, and OgM in 0.5%, and in about 2-3% no detectable M protein.
Recent diagnostic criteria have included specific biomarkers such as clonal bone marrow plasma cells equal or greater than 60%, serum free light chain ratio equals greater than 100, and one focal lesion on MRI imaging which was added to markers of end-stage organ damage- hypercalcemia renal insufficiency, anemia, or bone lesions.
At least 50% of patients with clonal plasma cell proliferation in monoclonal gammopathy of unknown significance (MGUS) translocations involving the immunoglobulin heavy chain (IgH) locus on chromosome 14q32 evolve into myeloma.