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.
What causes multiple myeloma? The short answer is that no one knows. The longer answer is that there are a number of factors that increase the risk of a MM diagnosis.
It can be argued that spending time trying to figure out what causes multiple myeloma is a waste of time. However, since I have MM and can identify possible causes multiple myeloma, then my son (and his children, etc. etc.) can take steps to reduce their risk of MM.
What are the known factors that increase the risk of multiple myeloma?
Changing age, gender and our race is difficult. But according to the two studies linked below, there are genetic risk factors that we can test for. If, for example, my son has the BCRA 1/2 gene, I would encourage him to undergo known lifestyle therapies that can reduce his risk of of MM such as
etc. While a genetic predisposition is not a guarantee to a MM diagnosis, it can increase the risk of getting MM.
Email me at David.PeopleBeatingCancer@gmail.com if you have questions about what causes multiple myeloma.
Thank you,
“Sometimes it seems much more is unknown about multiple myeloma than is known. Questions about what causes it and whether it’s an inherited disease remain unanswered, according to Jens Hillengass, MD, PhD, Chief of Myeloma at Roswell Park Comprehensive Cancer Center.
“No one knows,” says Dr. Hillengass about the cause. “There have been reports that it is more common among people in certain occupations, like painters and farmers. A condition called monoclonal gammopathy of undetermined significance (MGUS) is a precursor of the disease that has been more common in 9/11 firefighters…”
Abstract-First-degree relatives of patients with multiple myeloma are at increased risk for the disease, but the contribution of pathogenic germline variants (PGV) in hereditary cancer genes to multiple myeloma risk and outcomes is not well characterized.
To address this, we analyzed germline exomes in two independent cohorts of 895 and 786 patients with multiple myeloma. PGVs were identified in 8.6% of the Discovery cohort and 11.5% of the Replication cohort, with a notable presence of high- or moderate-penetrance PGVs (associated with autosomal dominant cancer predisposition) in DNA repair genes (3.6% and 4.1%, respectively).
PGVs in BRCA1 (OR = 3.9, FDR < 0.01) and BRCA2 (OR = 7.0, FDR < 0.001) were significantly enriched in patients with multiple myeloma when compared with 134,187 healthy controls.
Five of the eight BRCA2 PGV carriers exhibited tumor-specific copy number loss in BRCA2, suggesting somatic loss of heterozygosity. PGVs associated with autosomal dominant cancer predisposition were associated with younger age at diagnosis, personal or familial cancer history, and longer progression-free survival after upfront high-dose melphalan and autologous stem-cell transplantation (P < 0.01).
Human papillomaviruses (HPV) are small DNA tumor viruses, and are associated with epithelial neoplasias. Although HPV are believed to be exclusively permissive in terminally differentiated squamous cells, we have previously identified HPV sequences in lymphoid tissues of five patients.
Because this result suggested that the range of the host virus cells could include cells of lymphoid origin, we used PCR and in situ hybridization to analyze nonepithelial tissues of patients with multiple myeloma from two institutions.
A statistically significant association was established between HPV and multiple myeloma (p < 0.001). This study supports the hypothesis that HPV can infect lymphoid cells…”