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.
Why is it significant that vitamin D supplementation slows cellular senescence? Because chemotherapy causes cellular senescence. Or, to put it another way, chemotherapy can age you.
As MM survivors know, remissions and relapses mean chemotherapy after chemotherapy.
Full disclosure- this post is NOT about anti-aging, looking younger, etc., etc.
I am a long-term MM survivor. Like many MM patients, I underwent induction therapy followed by an autologous stem cell transplant. To say the least, this is a lot of chemotherapy, which means a lot of cellular senescence.
According to the study linked below, daily supplementation of vitamin D and omega-3 fatty acids may have slowed cellular senescence.
While I was blogging about the topic of nutritional supplementation slowing or reversing cellular senescence, I decided to ask ChatGPT if other supplements might offer the same properties of slowing aging.
Nutritional supplements that have shown potential to slow or reverse cellular senescence are primarily studied for their ability to affect oxidative stress, inflammation, DNA damage, mitochondrial function, and senescence-associated secretory phenotype (SASP). While research is still emerging (mostly in animals or in vitro), here are some of the most promising compounds, categorized by mechanism:
These help eliminate senescent cells, reducing their burden:
Fisetin
A flavonoid found in strawberries.
Has senolytic activity in mice and reduces age-related dysfunction.
Human trials are ongoing.
Quercetin + Dasatinib
Shown in preclinical and early clinical studies to selectively kill senescent cells.
Dasatinib is a cancer drug; quercetin is a flavonoid.
Used in combination in small human studies (e.g., idiopathic pulmonary fibrosis).
Piperlongumine
Derived from long pepper.
Shows senolytic activity in preclinical models.
These modulate the phenotype of senescent cells or prevent their harmful effects:
Curcumin
Anti-inflammatory and antioxidant.
Can suppress SASP and may delay onset of senescence.
Resveratrol
Found in grapes and red wine.
Activates SIRT1 and AMPK, mimicking calorie restriction.
Mixed evidence; may delay senescence in some models.
Nicotinamide Mononucleotide (NMN) / Nicotinamide Riboside (NR)
NAD+ precursors.
Boost mitochondrial function, DNA repair.
May reduce senescence by improving energy metabolism and activating sirtuins.
Metformin (technically a drug, not a supplement)
Activates AMPK, reduces inflammation and oxidative stress.
Delays senescence in several models.
Being studied in the TAME trial for aging.
Epigallocatechin Gallate (EGCG)
From green tea.
Antioxidant; inhibits SASP in some models.
May reduce senescence in endothelial cells and fibroblasts.
Spermidine
Promotes autophagy.
Associated with increased lifespan and healthspan in models.
May reduce cellular senescence by enhancing cellular housekeeping.
Astaxanthin
A powerful antioxidant carotenoid.
Shown to reduce oxidative stress–induced senescence in vitro.
Alpha-Ketoglutarate (AKG)
Metabolite involved in the Krebs cycle.
Supplemented AKG extends lifespan and reduces inflammatory markers in mice.
May reduce markers of senescence.
Coenzyme Q10 (CoQ10)
Mitochondrial support and antioxidant.
Reduces oxidative stress, potentially reducing senescence burden.
Most evidence is preclinical—in vitro or animal models.
Human trials are limited, often small or lacking rigorous endpoints.
Effectiveness likely depends on dose, delivery method, and individual biology.
Again, this is not an anti-aging post. My goal is to help MM survivors manage their incurable blood cancer. In this case, that means slowing cellular senescence.
Email me at David.PeopleBeatingCancer@gmail.com if you’d like to learn more about managing multiple myeloma.
Thank you,
David Emerson