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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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vitamin D supplementation slows cellular senescence

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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.



What nutritional supplements have been shown to slow or reverse cellular senescence?

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:


🧬 Senolytics (Clear Senescent Cells)

These help eliminate senescent cells, reducing their burden:

  1. Fisetin

    • A flavonoid found in strawberries.

    • Has senolytic activity in mice and reduces age-related dysfunction.

    • Human trials are ongoing.

  2. 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).

  3. Piperlongumine

    • Derived from long pepper.

    • Shows senolytic activity in preclinical models.


🛡️ Senomorphics (Suppress SASP and Senescent Phenotype)

These modulate the phenotype of senescent cells or prevent their harmful effects:

  1. Curcumin

    • Anti-inflammatory and antioxidant.

    • Can suppress SASP and may delay onset of senescence.

  2. Resveratrol

    • Found in grapes and red wine.

    • Activates SIRT1 and AMPK, mimicking calorie restriction.

    • Mixed evidence; may delay senescence in some models.

  3. Nicotinamide Mononucleotide (NMN) / Nicotinamide Riboside (NR)

    • NAD+ precursors.

    • Boost mitochondrial function, DNA repair.

    • May reduce senescence by improving energy metabolism and activating sirtuins.

  4. 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.

  5. Epigallocatechin Gallate (EGCG)

    • From green tea.

    • Antioxidant; inhibits SASP in some models.

    • May reduce senescence in endothelial cells and fibroblasts.


🧪 Other Promising Compounds

  1. Spermidine

    • Promotes autophagy.

    • Associated with increased lifespan and healthspan in models.

    • May reduce cellular senescence by enhancing cellular housekeeping.

  2. Astaxanthin

    • A powerful antioxidant carotenoid.

    • Shown to reduce oxidative stress–induced senescence in vitro.

  3. Alpha-Ketoglutarate (AKG)

    • Metabolite involved in the Krebs cycle.

    • Supplemented AKG extends lifespan and reduces inflammatory markers in mice.

    • May reduce markers of senescence.

  4. Coenzyme Q10 (CoQ10)

    • Mitochondrial support and antioxidant.

    • Reduces oxidative stress, potentially reducing senescence burden.


⚠️ Caveats

  • 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

  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

Vitamin D3 and Marine Omega-3 Fatty Acids Supplementation and Leukocyte Telomere Length: 4-Year Findings from the VITAL Randomized Controlled Trial

Background

Limited studies suggest that vitamin D or omega 3 fatty acids (n-3 FAs) supplementation may be beneficial for telomere maintenance, however, evidence from large randomized clinical trial is lacking. We hypothesized that vitamin D or n-3 FAs supplementation reduce leukocyte telomere length (LTL) attrition overtime by leveraging the VITamin D and OmegA-3 TriaL (VITAL) trial.

Methods

VITAL is a large, randomized, double-blind, placebo-controlled trial with a 2 x 2 factorial design of vitamin D3 (2,000 IU/day) and marine n-3 FAs (1 g/day) supplements for 5 years among a representative sample of 25,871 US females ≥55 and males ≥50 years of age.
The VITAL Telomere study (NCT04386577) included 1054 participants who were evaluated in person at the Harvard Clinical and Translational Science Center. LTL was determined by the Absolute Human Telomere Length Quantification quantitative Polymerase Chain Reaction (PCR) method at baseline, Year 2, and Year 4.
The pre-specified primary outcome measures were changes in LTL between baseline, Year 2 and Year 4. Analyses of intervention effect used mixed-effects linear regression models.

Results

LTL was measured in a total of 2,571 samples from the 1031 participants at baseline, year 2, and year 4. Compared to placebo, vitamin D3 supplementation significantly decreased LTL attrition by 0.14 kilo base pairs (kb) (0.01, 0.27) over 4 years (p = 0.039).
Overall trend analysis showed that the vitamin D3 supplementation group had LTLs that were about 0.035 kb higher per year of follow-up compared to placebo group (0.002, 0.07, p=0.037). Marine n-3 FAs supplementation had no significant effect on LTL at either year 2 or year 4.

Conclusion

4-years of supplementation with 2000 IU/day vitamin D3 reduced telomere attrition by 140 bp, suggesting that vitamin D3 daily supplementation with or without n-3 FAs might have a role in counteracting telomere erosion or cell senescence.

 

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