For all the Ehlors-Daniel Shyndrone suffers out there in the world, could this be beneficial for collagen health?
78
u/ACABiologist
From what I've read about ozempic it also causes neurogenesis. What else causes neurogenesis and joint repair, fasting. More research needs to be done on the mechanisms of the drug before these claims can be made. Is the ozempic causing joint repair or is a suppressed appetite triggering the body's natural repair processes?
31
u/En-TitY_
Wasn't there just a paper released showing it causes aggressive Thyroid cancer?
25
u/DaisiesSunshine76
I just found out I likely have rheumatoid arthritis. I wonder if this could someday be a treatment for me.
19
u/ItzLuzzyBaby
An observable 17% increase in cartilage thickness?? Alright time to get my 25 year old knees back
7
u/zambizzi
About to get cheaper, too:
https://www.cbc.ca/news/health/generic-ozempic-canada-waiting-9.7142339
I don’t take these drugs but I know people who are having success with it, and if it’s safe, good for them!
5
u/Excellent-Pain-5479
As someone who struggles with intense food noise, messed up satiety signals and has osteoarthritis, this could help me so much but nooo I won't get any prescribed bc I'm average weight 🫠 fml
4
u/boppy28
I have been on biologics for the last few years for psoriatic arthritis. About 18 months ago I started taking ozempic for diabetes (caused by all the prednisone use) and my body feels so much better. I'm due for a baseline scan in a few months so it will be interesting to see if I'm the same as last time or better. I know I won't be worse.
2
u/NightSail
Not sure if it was the weight loss, but I can walk down stairs using both knees instead of just the left one.
2
u/Thin-Honey892
Wait til they see the same results with a ketogenic diet. Your body will heal itself in the sustained absence of glucose.
2
u/Existing_Goal_7667
In mice, in a tiny pilot study. I won't hold my breath on this one.
1
u/uncle_stripe
Sounds very similar to the repair process that intermittent fasting can trigger. I wouldn't be surprised if this benefit is just because users are also in a fasted state.
1
u/lil_squib
Doesn’t weight loss on its own do this?
1
u/librocubicuralist
Does that mean Tirzepetide would do the same thing?
1
u/garcime
Any idea if this also happens with mounjaro?
1
u/Matshelge
Once we get this in oral form, or a patch, I suspect it will be as common as supplement and practically everyone will be using it.
1
u/HARCYB-throwaway
Ok now isolate the mechanism and let me repair my joints without all of the ozempic bullshit that comes along with it
1
u/TruthTeller6000
Or it could be the fact the person is getting skinnier so the joint has less stress?
WOW! This is amazing news 🙌 I have osteoarthritis in my knees and various places. I thought ny weight loss was the reason my knees stopped hurting. Amazing!
44
u/husbandchuckie
You’d think there would be more evidence with how many people have been taking these x rays mris anecdotal
3
u/supernitin
Amazing but also concerning they are discovering all this stuff it does after it has been made widely available- we hear about the good stuff… but can’t be all be good.
2
u/North-Profession4507
In mice. Read the fine print. In mice. I showed this study to my orthopedic surgeon, and he immediately pointed out it’s only been shown in mice. Transferring the results to humans is very difficult.
2
u/lylemcd
And if rat/mouse data every translated to humans this might matter.
And yet it fails to do so in roughly 99.99999% of cases
1
u/shk2096
The sample size for this study was n=20. Isn’t that quite low?
1
u/Speech-Language
Epic makes you look older, but I’d take that to heal my joints
It is all good info but you missed a very big culprit most physicians overlook.
Bacteria that causes gum disease is correlated with cardiovascular disease. Mechanisms unknown. Theories include bacteria causing vascular inflammation, autoimmune response to bacteria….
https://newsroom.heart.org/news/gum-disease-may-be-linked-to-plaque-buildup-in-arteries-higher-risk-of-major-cvd-events
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u/GarifalliaPapa
I am writing this for the other scientists who are interested in the aging science (advanced mechanisms):
Aortic and cardiovascular aging represent a convergence of structural degeneration, metabolic stress, and signaling dysregulation that progressively impair vascular function. The aorta stiffens due to elastin fragmentation, collagen accumulation and cross-linking (especially via advanced glycation end-products, AGEs), endothelial dysfunction, mitochondrial decline, chronic inflammation, and calcium deposition. This process accelerates notably between ages 45–55, when repair capacity declines and cumulative damage crosses a threshold. Mechanistically, arterial stiffness increases pulse wave velocity, elevates systolic blood pressure, and amplifies mechanical stress on organs, creating a systemic feedback loop that accelerates aging and disease.
At the structural level, elastin degradation is essentially irreversible because elastin turnover is extremely low after early life. As elastin fibers fragment, collagen becomes the dominant load-bearing component, but collagen is inherently stiffer, especially when cross-linked by AGEs formed under hyperglycemic and oxidative conditions. This shift transforms arteries from elastic reservoirs into rigid conduits. Simultaneously, vascular smooth muscle cells (VSMCs) undergo phenotypic switching toward osteogenic-like states, promoting calcification. These structural changes are tightly coupled with molecular signaling pathways such as TGF-β, NF-κB, and oxidative stress cascades.
Endothelial dysfunction is a central initiating event in vascular aging. The endothelium regulates vascular tone through nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS). With aging, oxidative stress reduces NO bioavailability by converting it into peroxynitrite, while inflammation suppresses eNOS activity. The result is impaired vasodilation, increased vascular tone, and pro-inflammatory signaling. Endothelial cells also become more adhesive, promoting leukocyte infiltration and early atherogenesis. Restoration of endothelial function is therefore one of the highest-leverage interventions.
Mitochondrial dysfunction within vascular cells amplifies these processes. Damaged mitochondria produce excess reactive oxygen species (ROS), which directly damage elastin, collagen, and endothelial cells while also activating inflammatory pathways such as NF-κB. Mitochondrial DNA damage further impairs energy production, limiting repair processes in the vessel wall. This creates a feedback loop where mitochondrial decline drives oxidative stress, which in turn accelerates vascular aging and stiffness.
Exercise is one of the most potent modulators of vascular aging because it directly targets multiple mechanisms simultaneously. Aerobic exercise increases shear stress on vessel walls, which upregulates eNOS and boosts nitric oxide production, restoring vasodilation. It also activates AMPK and PGC-1α, promoting mitochondrial biogenesis and reducing ROS. High-intensity interval training (HIIT) further enhances vascular responsiveness and aortic distensibility by inducing transient metabolic stress that triggers adaptive repair pathways. Resistance training complements this by improving insulin sensitivity and reducing systemic inflammation. The combined effect is a measurable reduction in arterial stiffness, often equivalent to reversing decades of vascular aging.
Dietary patterns exert long-term control over vascular integrity through metabolic and inflammatory pathways. Time-restricted feeding and caloric restriction activate AMPK and SIRT1, improving mitochondrial efficiency, reducing oxidative stress, and enhancing endothelial function. Mediterranean and DASH diets provide polyphenols, healthy fats, and micronutrients that suppress inflammation, improve lipid profiles, and support NO production. Importantly, dietary fiber and fermented foods modulate the gut microbiome, reducing production of trimethylamine N-oxide (TMAO), a metabolite linked to atherosclerosis, fibrosis, and vascular stiffness. This highlights a critical gut–vascular axis in aging biology.
Blood pressure and glucose control are fundamental because mechanical and biochemical stress directly damage arterial structure. Chronic hypertension increases shear and tensile stress, accelerating elastin breakdown and collagen deposition. Hyperglycemia promotes AGE formation, stiffening the vascular matrix and impairing endothelial signaling. Maintaining optimal levels (<120/80 mmHg and low fasting glucose) preserves vascular elasticity. Compounds like metformin and berberine improve insulin sensitivity and reduce inflammatory signaling, indirectly protecting the aorta, while magnesium inhibits vascular calcification by regulating calcium handling in smooth muscle cells.
Nitric oxide–enhancing strategies directly target endothelial dysfunction. Dietary nitrates from beets and leafy greens are converted into nitrite a
14
u/255cheka
another amazing piece. thank you. anybody have thoughts on garlic/garlic extract? seen a small amount of evidence it can help clean out blood vessels
5
u/Blud_Klot
You know, the top comment nailed it. Maintaining optimal health feels like a second job these days. I've been taking meo nutrition berberine for a third a year now specifically for the cardiovascular benefits you mentioned. What do you know? My last checkup showed better numbers across the board.
1
u/GarifalliaPapa
Best scientific research:
[1] Aging Acceleration Around Age 50 and Organ-Specific Decline Patterns https://www.nature.com/articles/d41586-025-02333-z
[2] Study Identifies Midlife Turning Point When Biological Aging Accelerates https://www.sciencealert.com/study-reveals-turning-point-when-your-bodys-aging-accelerates
[3] Effects of Exercise on Arterial Stiffness and Vascular Health https://tensiomed.com/exercise-and-arterial-stiffness/
[4] High-Intensity Interval Training Improves Atrial Function and Reduces Aortic Stiffness (RCT) https://pubmed.ncbi.nlm.nih.gov/32529506/
[5] Impact of High-Intensity Interval Training on Cardiac Mechanics and Aortic Stiffness https://repository.canterbury.ac.uk/item/8vw97/left-atrial-mechanics-and-aortic-stiffness-following-high-intensity-interval-training-a-randomised-controlled-study
[6] Time-Restricted Feeding Association with Arterial Aging and Cardiovascular Health https://pmc.ncbi.nlm.nih.gov/articles/PMC10318230/
[7] Mediterranean Diet Effects on Arterial Stiffness and Vascular Function https://pmc.ncbi.nlm.nih.gov/articles/PMC11990623/
[8] TMAO and Its Role in Age-Related Cardiovascular Dysfunction https://pmc.ncbi.nlm.nih.gov/articles/PMC12572090/
[9] Metformin’s Protective Effects Against Aortic Stiffness and Vascular Aging https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2021.721213/full
[10] Vitamin K2 and Vitamin D Supplementation Effects on Coronary Artery Health https://pmc.ncbi.nlm.nih.gov/articles/PMC11198368/
[11] Nutritional Strategies to Enhance Nitric Oxide Production and Vascular Function https://pmc.ncbi.nlm.nih.gov/articles/PMC9710401/
[12] Dietary Polyphenols and Their Effects on Reducing Arterial Stiffness https://pmc.ncbi.nlm.nih.gov/articles/PMC6471395/
[13] Fisetin as a Senotherapeutic Extending Healthspan and Lifespan https://pubmed.ncbi.nlm.nih.gov/30279143/
[14] Combined Effects of Curcumin and Omega-3 on Inflammation and Joint Health https://pmc.ncbi.nlm.nih.gov/articles/PMC12265326/
[15] Role of Vitamin C and Lysine in Cardiovascular Health and Tissue Integrity https://naturalfoodpantry.ca/blogs/health-conditions/why-you-need-vitamin-c-and-lysine-for-heart-health-and-more
[16] NAD+ Precursors Reverse Endothelial Dysfunction and Improve Vascular Health https://www.nmn.com/news/nad-precursors-endothelial-inflammation-dysfunction
[17] Pyrroloquinoline Quinone (PQQ) and Its Potential Anti-Aging Effects https://www.lifeextension.com/magazine/2020/5/how-pqq-slows-aging
[18] Benfotiamine and Its Role in Metabolic and Vascular Health https://www.drperlmutter.com/wp-content/uploads/2021/06/10-Benfotiamine_FALL_03n.pdf
[19] Auricular Vagus Nerve Stimulation Reduces Heart Rate and Improves Autonomic Function https://pmc.ncbi.nlm.nih.gov/articles/PMC11862327/
I am writing this for the other scientists who are interested in the aging science (advanced mechanisms):
DNA damage can be understood as a central, system-level driver of aging because it represents the cumulative burden of molecular errors that cells fail to fully repair over time. Both endogenous sources (such as mitochondrial reactive oxygen species and replication stress) and exogenous sources like UV radiation and toxins continuously generate lesions in nuclear and mitochondrial DNA. Aging emerges when the rate of damage exceeds the capacity of repair systems, leading to genomic instability, disrupted gene expression, and progressive loss of cellular function. Importantly, DNA damage is not passive; it actively triggers stress-response pathways such as p53 and ATM/ATR, driving cells toward senescence or apoptosis and amplifying aging processes.
The types of DNA damage are diverse and differ in severity and biological consequences. Single-strand breaks are frequent and usually repairable, while double-strand breaks are highly dangerous and can lead to mutations or chromosomal rearrangements. Oxidative base modifications, such as 8-oxoG, accumulate under conditions of oxidative stress, while chemical adducts and crosslinks arise from environmental exposures. Telomeres are particularly vulnerable due to their structure and replication limitations. Mitochondrial DNA is even more susceptible because it is located near the electron transport chain, a major source of reactive oxygen species, and has relatively limited repair capacity compared to nuclear DNA.
To counteract this constant damage, cells rely on a sophisticated network of DNA repair systems. Base excision repair corrects small oxidative lesions, while nucleotide excision repair removes bulky DNA distortions such as those caused by UV light. Double-strand breaks are repaired either by non-homologous end joining, which is rapid but error-prone, or homologous recombination, which is accurate but limited to certain phases of the cell cycle. PARP1 acts as a key sensor of single-strand breaks and uses NAD+ to recruit repair machinery, while sirtuins such as SIRT1 and SIRT6 regulate chromatin structure and enhance repair efficiency. Together, these pathways form the core defense architecture that preserves genomic integrity.
DNA damage becomes particularly harmful because it participates in a self-reinforcing feedback loop that accelerates aging. Accumulated damage activates the DNA damage response, which triggers p53/p21 signaling and leads to cellular senescence. Senescent cells then secrete inflammatory factors known as the senescence-associated secretory phenotype (SASP), increasing systemic inflammation. This inflammation raises reactive oxygen species levels, which in turn cause further DNA damage. At the same time, DNA damage contributes to epigenetic drift, disrupting gene regulation and further impairing repair capacity. This cycle creates a progressive escalation of dysfunction across tissues.
Strong causal evidence for the importance of DNA repair comes from progeroid syndromes and comparative biology. Disorders such as Cockayne syndrome, Werner syndrome, and Progeria involve defects in DNA repair pathways and produce accelerated aging phenotypes, including neurodegeneration and tissue failure. In contrast, long-lived species like naked mole rats and bowhead whales exhibit enhanced DNA repair mechanisms or expanded repair gene networks, correlating with exceptional longevity. Human centenarians also tend to show higher expression of repair enzymes such as PARP1 and Ku70, supporting the link between efficient DNA maintenance and extended lifespan.
A critical regulator of DNA repair capacity is NAD+, a metabolic cofactor required by both PARP enzymes and sirtuins. As NAD+ levels decline with age, the efficiency of DNA repair decreases. NAD+ precursors such as NMN and NR restore intracellular NAD+ pools, reactivating PARP1-mediated repair and sirtuin-driven genomic stabilization. In preclinical models, this results in reduced DNA damage, improved mitochondrial function, and partial reversal of age-related phenotypes. This places NAD+ metabolism at the center of the connection between energy balance and genome maintenance.
Beyond direct repair, DNA integrity is also influenced by epigenetic regulation. DNA damage disrupts chromatin organization and leads to loss of epigenetic information, a process sometimes described as “epigenetic noise.” Partial cellular reprogramming using Yamanaka factors has demonstrated that it is possible to reset epigenetic marks and restore youthful gene expression patterns without fully dedifferentiating cells. Mechanistically, this involves chromatin remodeling, improved localization of repair proteins, and enhanced genome stability. These findings suggest that aging is driven not only by accumulated damage but also by a loss of regulatory information that governs repair processes.
Lifestyle factors play a maj
11
u/toponico11
so i should def be injecting NAD+ or what?
5
u/Jinxysw
To incorporate fasting, what does a proper fast look like? Does it count if youre sleeping?
3
u/ZombiezzzPlz
Don't forget Epithalon and if you're talking mitochondria repair add in MOTS-C and SS-31 peptides. Oral supplements aren't going to do a lot for you
3
u/hawkedmd
Although Polypodium leucotomas has good evidence for skin DNA protection, anyone have any thoughts on possibility of more generalized benefits against non-UV damage?
1
u/Agile_Butterfly6091
had the same issue with fatigue and brain fog, thought it was just getting older. started taking meo nutrition celluvate about 2 months ago and honestly feel sharper than I have in years. the NR dose is way higher than most supplements I looked at.
1
u/GarifalliaPapa
Best scientific research:
[1] DNA Damage as a Potential Unifying Cause of Aging https://www.cecad.uni-koeln.de/outreach/news/article/dna-damage-the-unifying-cause-of-aging
[2] Epigenomic Signatures of Accelerated Aging in Progeroid Syndromes https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13959
[3] Enhanced DNA Repair Mechanisms in Naked Mole Rats and Longevity https://lifespan.io/news/why-naked-mole-rats-have-better-dna-repair/
[4] Experimental Reversal of DNA Aging in Mice https://www.sciencealert.com/scientists-have-successfully-reversed-dna-ageing-in-mice
[5] Effectiveness of NAD⁺ Boosters (NR, NMN) on Cellular Aging and DNA Repair https://www.gethealthspan.com/research/article/nad-boosters
[6] DNA Damage Theory of Aging: Overview and Mechanisms https://en.wikipedia.org/wiki/DNA_damage_theory_of_aging
[7] Lifestyle and Dietary Strategies to Protect DNA from Damage https://www.cleaneatingmag.com/clean-diet/general-health/11-genius-science-backed-ways-to-save-your-dna/
[8] Effects of Fasting on FOXO3 Expression and Longevity Pathways https://pmc.ncbi.nlm.nih.gov/articles/PMC9883274/
[9] Role of Melatonin and Sleep in DNA Repair and Oxidative Stress Reduction https://foodmedcenter.org/can-sleep-and-melatonin-repair-your-dna-new-research-reveals-how-melatonin-supplementation-diet-and-lifestyle-changes-can-enhance-dna-repair-fight-oxidative-stress-and-protect-long-term-health/
[10] Melatonin Supplementation and Its Effects on Antioxidant Status https://pubmed.ncbi.nlm.nih.gov/29165732/
[11] N-Acetylcysteine (NAC) Promotes DNA Repair After Genotoxic Damage https://biomedres.us/fulltexts/BJSTR.MS.ID.004776.php
[12] Mechanisms of N-Acetylcysteine in Preventing DNA Damage https://pubmed.ncbi.nlm.nih.gov/11408342/
[13] Vitamin D and Its Receptor in Regulation of DNA Repair Pathways https://pmc.ncbi.nlm.nih.gov/articles/PMC5050051/
[14] Vitamin D Modulates Expression of DNA Repair Genes https://pubmed.ncbi.nlm.nih.gov/33588040/
[15] Magnesium Deficiency and Its Role in DNA Damage and Genomic Instability https://www.nutrunity.com/updates/magnesium-deficiency-and-dna-damage
[16] Resveratrol and Quercetin Enhance NAD⁺-Mediated DNA Repair Mechanisms https://journals.sagepub.com/doi/full/10.1177/1934578X211045465
[17] Effects of Coenzyme Q10 and Curcumin on Oxidative Stress and DNA Protection https://discovery.dundee.ac.uk/en/publications/the-effects-of-coenzyme-q10-and-curcumin-supplementation-in-freez/
[18] Sauna Use and Its Potential Effects on Longevity and Cellular Stress Response https://hyperthermicwellness.com/effects-of-sauna-use-on-longevity-2/
[19] Molecular Mechanisms of DNA Damage Response and Epigenetic Regulation in Aging https://pmc.ncbi.nlm.nih.gov/articles/PMC12651117/
[20] Hypothesis: DNA Damage as the Primary Cause of Aging and Target for Reversal https://www.reddit.com/r/immortalists/comments/1j6u11k/aging_is_caused_primarily_by_dna_damage_by/
160-240mg Telmisartan is a god send for mood and anhedonia, everytime it makes me feel great, most unique compound ever, feel similar to how pioglitazone affect me (PPAR-gamma)
9
u/Mialuvailuv
As someone with ADHD, genetic predisposition to Parkinson's, Alzheimers, and whom has DD-genotype ACE ("ACE Deletion"), there has never been a single treatment that has made a bigger difference in every aspect of my life than Telmisartan.
By every measure it has improved my quality of life; mental, physical, emotional. I've been on it for five months now, and I hope to continue using it forever. I had to take one month off of it because of an insurance issue and switch back to valsartan, and the difference was easily noticeable within two days. I didn't sleep through the night for weeks.
9
u/acattackISback
What's the summary/takeaway? I don't understand how it is a nootropic...
3
u/Western_Extent_9764
Telmisartan doesnt stop erythropoiesis as strongly as enalapril. If im on androgens id go with the enalapril to slow down blood volume and pressure.