RE: Epigenetische Reprogrammierung - 9

Das Einfachheit halber nenne ich das Tier "Unsterbliche Qualle" (UQ), der wissenschaftliche Name lautet Turritopsis dohrnii. Die UQ kann sich real verjüngen und wieder altern. Damit ist sie der einzig bekannte tierische Organismus, der für uns als Modell für die Unsterblichkeit infrage kommt.



Leider sind die Bezeichnungen der verschiedenen Stadien etwas uneinheitlich. Bei der folgenden Studie sind diese hilfreich für's Verständnis (nicht übersetzt):

Polyp (siehe 4. im Bild)
Cyst (nächstältere Zwischenstufe)
Medusa (Bezeichnet die ausgewachsene Qualle)

Die Studie aus der die nachfolgenden Zitate stammen (sofern nicht anders angegeben):
Cellular Reprogramming and Immortality: Expression Profiling Reveals Putative Genes Involved in Turritopsis dohrnii’s Life Cycle Reversal
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8480191/

Dort wird noch zwischen "Colonial Polyp" und "Reversed Polyp" unterschieden, was die gleiche Stufe zu unterschiedlichen Zeitpunkten (bzw. mit unterschiedlichem Ursprung) darstellen sollte ("from colonial polyp to medusa, to cyst, to reversed polyp").
Ferner: "analysis of the life cycle stages involved in reverse development (...) was performed in the following sequence: 1) Colonial Polyp, 2) Medusa, 3) Cyst, and 4) Reversed Polyp. This sequence reflects the natural ontogenetic trajectory observed in T. dohrnii during its life cycle reversal."

Wikipedia bestätigt die Verjüngungsreihenfolge Medusa -> Cyst -> Polyp (wie oben, nur umgekehrt):

Zitat

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Experiments have revealed that all stages of the medusae, from newly released to fully mature individuals, can transform back into polyps under the conditions of starvation, sudden temperature change, reduction of salinity, and artificial damage of the bell with forceps or scissors.[3] The transforming medusa is characterized first by deterioration of the bell, mesoglea, and tentacles. All immature medusa (with 12 tentacles at most) then turned into a cyst-like stage and then transformed into stolons and polyps. However, about 20%-40% of mature medusa went into the stolons and polyps stage without passing the cyst-like stage.

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https://en.wikipedia.org/wiki/Turritopsis_dohrnii

Nun will man ja nicht wieder zum Embryo werden, also legen wir ein besonderes Augenmerk auf den Übergang Medusa -> Cyst. Es stellte sich raus, dass von den Top 50 Genen, die bei der Reprogrammierung besonders exprimiert waren, viele unbekannt sind:

Zitat

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The 44% among the top 50 DEGs being novel is a striking comparison to the 20.7% of unannotated sequences in the overall transcriptome. The most significant DEG among the 224 genes was a gene with no annotation (Td_DN103197_c0_g1). It had no evidence of any expression in all T. dohrnii samples except for the Cyst replicates (fig. 3A). Additionally, there were other unannotated genes that showed a significant peak at the Cyst, such as gene Td_DN92408_c0_g2 (fig. 3B).

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DEGs = differentially expressed genes

Ist das unser Verjüngungs-Gen?

Zitat

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We report genes involved in lifespan and aging (i.e., “Serine-racemase-like” and “Peptide methionine sulfoxide reductase-like [MsrA])” and in transposition and DNA integration (table 1 and fig. 2C–F). Among them is “Transposable element Tc3 transposase,” largely explored in Caenorhabditis elegans as one of the most active transposons (Bessereau 2006). Genes associated to DNA repair and response to DNA damage, such as Ubiquitin-related genes, proteins that target cellular destruction by proteasomes in response to DNA damage, were also found in Cluster 5 (table 1 and fig. 2G). Several cancer and tumor-related genes were also reported. Among them were “Breast cancer type 1 susceptibility protein isoform X1 BRCA1),” “Tumor protein p63-regulated gene 1-like protein (TPRG1L),” and “Tumor necrosis factor receptor superfamily member 16-like (Tnfrsf16)” (supplementary Appendix F, Supplementary Material online and fig. 2H).

Finally, we report numerous genes associated with cell/tissue differentiation and development, such as “Protein PEV” and “Methionine aminopeptidase 2” with functions related to cell fate determination and embryonic development, respectively (table 1 and fig. 3I and J). A functional gene enrichment analysis of Cluster 5 reported that terms associated with larval development, the response to DNA damage, and protein monoubiquitination were among the most enriched (supplementary Appendix E, Supplementary Material online).

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Also macht die UQ bei ihrer Verjüngung so ziemlich alles, das hier bereits überlegt wurde: Epigenetische Verjüngung (mit den unbekannten Genen?), beschädigte Zellen entfernen, Krebs vorbeugen, DNA-Reparatur, Transposonen managen, und so weiter. Jetzt wäre doch wirklich interessant, was diese unbekannten Gene machen und was passieren würde, wenn man aus den unbekannten und bekannten involvierten Genen eine Medizin zur Verjüngung entwerfen würde! Das geht sicher nicht ohne weiteres, aber probieren könnte man es ja mal (an Mäusen oder so). Danach passt man es stufenweise an, bis die Wirkung stimmt. Was hindert die Forschung daran, dies zu versuchen?

Hier noch eine neuere Studie:

Genome assembly and transcriptomic analyses of the repeatedly rejuvenating jellyfish Turritopsis dohrnii

Zitat

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The predicted genes were categorized into three groups, namely high confidence (HC), low confidence (LC), and transposable element (TE).
(...)
On the other hand, few HC genes hit to the human pluripotent stem cell markers including iPS Yamanaka factors,39 such as LIN28, SSEA1, KLF4, OCT3, SOX2, and NANOG. These results suggest that the no-hit genes in the UniProtKB analysis could contribute significantly to the dedifferentiation and redifferentiation cycle of Turritopsis during rejuvenation and regeneration, and that dedifferentiation of Turritopsis might be controlled by different mechanisms of human.
(...)
Finally, although we here performed the GO enrichment analysis, it was difficult to reach any definitive conclusions in regard to the relationships between the characteristics of T. dohrnii and gene functions. Currently, we are trying to single-cell RNA-Seq and bulk RNA-Seq analyses to find clues to the mechanisms underlying rejuvenation.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9835754/

Die Autoren vermuten also, dass die Verjüngung der Unsterblichen Qualle anders funktionieren könnte als beim Menschen, bzw. nicht über Yamanaka-Faktoren. Soweit mir bekannt ist die Verjüngung mit Yamanaka-Faktoren insofern auch beim Menschen "künstlich", als dass diese vom Körper selbst so nicht dafür eingesetzt werden, oder?

Hallo,

die Mitochondrien steuern die Epigenetik der Zellen: https://www.youtube.com/watch?v=YZu8kqDtjjE .

Viele Grüße

Roger

#202
Dass Menschen als Teil ihres "normalen Lebenszyklus" nicht verjüngen, ist ja keine neue Erkenntnis.
Vielleicht gibt es im Prinzip immer noch (?) den Mechanismus für eine Verjüngung, der wird aber durch irgendeine Veränderung in der Evolution ausgeschaltet.
Genauso wie der Mensch mglw. noch die Gene dafür hat, einen Schwanz zu haben, aber diese nicht mehr eingesetzt werden.

#204
Wann tritt das denn im erwachsenen Gewebe auf?

Targeted partial reprogramming of age-associated cell states improves markers of health in mouse models of aging
https://www.science.org/doi/abs/10.1126/...-2IiCDaCpfUxKJg

In vivo neuron-specific expression of C. elegans reprogramming factor orthologs does not alleviate age-related cognitive decline
https://micropublication.org/journals/bi...n8tV_nSCVQtseeg

Zitat von Speedy im Beitrag #208

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In vivo neuron-specific expression of C. elegans reprogramming factor orthologs does not alleviate age-related cognitive decline
https://micropublication.org/journals/bi...-biology-001304

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Zitat

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It is possible that pluripotency is regulated differently in C. elegans than in other species; we do not favor this hypothesis, however, as the OSK(M) pluripotency factors are widely conserved from mammals to invertebrates (Rosselló et al., 2013) and the worm OSK orthologs are required for a cellular transdifferentiation event that occurs during larval development (Kagias et al., 2012). Our results contrast with the dramatic regeneration and rejuvenation of injured or aged mouse post-mitotic retinal ganglion cells (RGCs) by OSK (Lu et al., 2020). This rejuvenation is dependent upon DNA demethylation (Lu et al., 2020), and depletion of the DNA cytosine methyltransferase DNMT3a is sufficient to induce RGC regeneration (Tai et al., 2023). As C. elegans lacks cytosine methylation (Simpson et al., 1986), the absence of apparent benefit of this intervention in worms raises the hypothesis that the benefits of OSK may be specific to organisms and cell types in which changes in DNA methylation contribute to the aging process. Taken together, our work suggests that future research on the efficacy of OSK(M) in cognitive aging may be best targeted at neurogenic processes, rather than in restoring healthy functions to aging neurons.

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Modulating DNA Polα Enhances Cell Reprogramming Across Species
https://www.biorxiv.org/content/10.1101/...FVLeZbZuMFJegPg

‘Yamanaka factors are a biological cheat code’

Zitat

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“Many patients, including my own family members, can’t afford to wait 5-10 years for new therapies to become available,” he says. “We’re committed to bridging the gap between cutting-edge research and patient care. While there are risks, such as teratomas in partial reprogramming, we believe these can be managed, especially when weighed against the potential benefits for patients with limited options.”

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https://longevity.technology/news/yamana...cal-cheat-code/

Kommentar: Endlich hat es mal jemand verstanden. Bleibt zu hoffen, dass sie Erfolg haben werden!

Wobei es schon schön wäre, noch mehr Forschung wie #141 zu sehen. Mit #141 und #143 könnte man sich ja theoretisch vielleicht sogar seine eigene epigenetische Verjüngung basteln (analog zum "Wir haben noch Essen zu Hause" von früher ). Aber ohne wenigstens einen Tierversuch dazu zu sehen, wäre das ein hohes Risiko.

TL;DR: Könnte man eine einfache epigenetische Verjüngung mit lediglich RepSox, Valproinsäure und Vitamin C erreichen?

Kurzer Recap: OSKM = OCT4, SOX2, KLF4, und MYC

RepSox führt zur Exprimierung von Oct4 und L-Myc (ähnlich cMyc):

RepSox effectively promotes the induced differentiation of sheep fibroblasts into adipocytes via the inhibition of the TGF-β1/Smad pathway

Zitat

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RepSox markedly promoted the expression of Oct4 (4.5-fold, Fig. 4D); however, Sox2 and Nanog expression were not detected (Fig. 4A and B), which indicated that the activation of Oct4 may play a crucial role in the acquisition of cell multipotency. These results also suggested that RepSox did not replace Sox2 by directly activating endogenous Sox2. By contrast, it was found that RepSox did increase the expression of L-Myc by 5-fold, which is a close homolog of cMyc that can functionally replace it in reprogramming. Therefore, although RepSox probably functions at the level of the initial somatic cell population to replace Oct4 and cMyc, it does not act by replacing Sox2 and Nanog.

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Valproinsäure scheint zumindest unter gewissen Bedingungen auch Klf4 zu aktivieren:

Evaluating the Differential Effects of Valproic Acid on Wharton’s Jelly Mesenchymal Stem Cells

Zitat

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Collectively, we demonstrated an increased (P < 0.05) c-Myc and Klf-4 expression in WJMSCs

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773934/

Das Paper scheint auch low dose Valproinsäure zu favorisieren.

Wenn ich das richtig lese, kann man mit Valproinsäure und Vitamin C auch Sox2 aktivieren:

Vitamin C- and Valproic acid-Induced Fetal Retinal Pigment Epithelial Stem-like Cells Recover Retinal Degeneration via Regulating SOX2
https://www.researchgate.net/publication...Regulating_SOX2

Was mich an Valproinsäure aber wirklich abschreckt, ist dass sie über Oxidation wirken könnte und dadurch DNA-Schäden verursacht:

Combined Transcriptomics and Chemical-Genetics Reveal Molecular Mode of Action of Valproic acid, an Anticancer Molecule using Budding Yeast Model

Zitat

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and thus supports our hypothesis of VA induced DNA damage. In response to DNA damage or DNA replication stress, Mec1/Rad53/Dun1 checkpoint kinase cascade activates several repair mechanisms

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https://www.nature.com/articles/srep35322

Hier noch eine neuere Studie, bei der Astrozyten zu OPCs (Progenitorzellen) rückprogrammiert wurden:

Conversion of Astrocyte Cell Lines to Oligodendrocyte Progenitor Cells Using Small Molecules and Transplantation to Animal Model of Multiple Sclerosis

Zitat

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Astrocytes, the most prevalent cells in the central nervous system (CNS), can be transformed into neurons and oligodendrocyte progenitor cells (OPCs) using specific transcription factors and some chemicals. In this study, we present a cocktail of small molecules that target different signaling pathways to promote astrocyte conversion to OPCs. Astrocytes were transferred to an OPC medium and exposed for five days to a small molecule cocktail containing CHIR99021, Forskolin, Repsox, LDN, VPA and Thiazovivin before being preserved in the OPC medium for an additional 10 days. Once reaching the OPC morphology, induced cells underwent immunocytofluorescence evaluation for OPC markers while checked for lacking the astrocyte markers. To test the in vivo differentiation capabilities, induced OPCs were transplanted into demyelinated mice brains treated with cuprizone over 12 weeks. Two distinct lines of astrocytes demonstrated the potential of conversion to OPCs using this small molecule cocktail as verified by morphological changes and the expression of PDGFR and O4 markers as well as the terminal differentiation to oligodendrocytes expressing MBP. Following transplantation into demyelinated mice brains, induced OPCs effectively differentiated into mature oligodendrocytes. The generation of OPCs from astrocytes via a small molecule cocktail may provide a new avenue for producing required progenitors necessary for myelin repair in diseases characterized by the loss of myelin such as multiple sclerosis.

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https://pubmed.ncbi.nlm.nih.gov/38594388/

CHIR99021: Siehe #144, Zusammenhang mit Zellidentität*/Pluripotenz.
Forskolin: Siehe #144
RepSox: Siehe oben
LDN: (wahrscheinlich) LDN-193189, Inhibitor des BMP pathways. Scheint genutzt worden zu sein, um die Zelldifferenzierung zu unterdrücken(?) Sehe hier auch eher Zellidentitäts*-Kontext.
VPA: Valproinsäure (siehe oben)
Thiazovivin: Rho kinase Inhibitor, braucht man vielleicht vor allem für Zellidentitäts*-Kontext?

* Gemeint ist der Verlust ebendieser, wodurch die betreffenden Stoffe für eine epigenetische Verjüngung womöglich weniger interessant sein könnten.

Faszinierend übrigens auch die Wirkung von Klf4 (das K in OSKM) auf die Mitochondrien:

Krüppel-like factor 4 (KLF4) induces mitochondrial fusion and increases spare respiratory capacity of human glioblastoma cells

Zitat

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KLF4 has been reported previously to promote mitochondrial biosynthesis in cardiac cells, but the effect of KLF4 on mitochondrial dynamics has not been reported. Here, we try to understand why U87 glioblastoma cell mitochondria fuse upon KLF4 expression. Mitochondria undergo fusion when they are facing stressful conditions (19); and one of the biological functions of mitochondrial fusion is to repair damaged mitochondria (20). For example, during normal metabolism and ATP production, mitochondria produce a large quantity of ROS that damage the mitochondrial genetic material. Mitochondrial fusion is critical for the exchange of their genetic material that can repair damaged DNA through recombination (21).

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https://www.jbc.org/article/S0021-9258(20)39751-9/fulltext

Hier noch ein Bericht von jemandem, der es u.a. mit Apigenin probiert hat:

How I Reversed My Biological Age by 13 Years: Yamanaka Factors and Apigenin Explained
https://www.reddit.com/r/Biohackers/comm...ge_by_13_years/

https://www.youtube.com/watch?v=DGSM1zfM55U

Müsste man sich mal genauer durcharbeiten, aber das wäre ja evtl. eine (vergleichsweise) risikoarme und kostengünstige Möglichkeit.

Edit: Das Video klingt schon sehr nach VT, auch das Feedback auf Reddit ist gemischt.

#214 Die einfachste Variante dazu:

500mg Curcumin
600mg Tributryn
B12
Multivitamin (optional, empfohlen)

Eine Stunde warten

300mg Apigenin (liposomal)
500mg NAD oder NMN
500mg Tributryn ("another half a gram", 600mg wie vorher wären also wohl auch okay)

Das ganze max. 2 mal täglich. Eine Woche on, dann eine Woche off (Pause).

Quelle: https://i.4pcdn.org/pol/1717465050629414.png

Leider kann man in diesem Thread irgendwie keine Bilder anhängen, sonst hätte ich es hochgeladen. Der Autor des Reddit-Threads hat es anscheinend auch nur von 4Chan übernommen, hat das Protokoll also nicht entworfen. Der tatsächliche Erfinder wiederum wirkt in seinen Videos leicht paranoid, was ja aber nicht heißen muss, dass das Protokoll wirkungslos ist. Da ich sebst mit Selleriesaft schon kleinere Erfolge erzielt habe, finde ich Apigenin durchaus interessant. Tributryn als HDACi ist ja auch nur eine andere Form von Butryat, welches hier gestern schon diskutiert wurde.

Noch ein paar Stoffe, die man sich anschauen könnte: Glabridin, Licochalcone D, Chrysoeriol (Luteolin-Derivat), Kaempferol, Quercetin, Icaritin (ein Stoff aus der Elfenblume; nicht Icaridin), Glucosamin und Silibinin.

The Flavonoid Glabridin Induces OCT4 to Enhance Osteogenetic Potential in Mesenchymal Stem Cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5733956/

https://en.wikipedia.org/wiki/Glabridin

Acceleration of Mesenchymal-to-Epithelial Transition (MET) during Direct Reprogramming Using Natural Compounds

Zitat

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Small molecules can enhance reprogramming. Licochalcone D (LCD), a flavonoid compound present mainly in the roots of Glycyrrhiza inflata, acts on known signaling pathways involved in transcriptional activity and signal transduction, including the PGC1-α and MAPK families. In this study, we demonstrated that LCD improved reprogramming efficiency. LCD-treated iPSCs (LCD-iPSCs) expressed pluripotency-related genes Oct4, Sox2, Nanog, and Prdm14. Moreover, LCD-iPSCs differentiated into all three germ layers in vitro and formed chimeras. The mesenchymal-to-epithelial transition (MET) is critical for somatic cell reprogramming. We found that the expression levels of mesenchymal genes (Snail2 and Twist) decreased and those of epithelial genes (DSP, Cldn3, Crb3, and Ocln) dramatically increased in OR-MEF (OG2+/+/ROSA26+/+) cells treated with LCD for 3 days, indicating that MET effectively occurred in LCD-treated OR-MEF cells. Thus, LCD enhanced the generation of iPSCs from somatic cells by promoting MET at the early stages of reprogramming.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9668095/

Chrysoeriol Improves In Vitro Porcine Embryo Development by Reducing Oxidative Stress and Autophagy

Zitat

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Chrysoeriol (CHE) is a flavonoid substance that exists in many plants. It has various physiological and pharmacological effects, including anti-inflammatory, antioxidant, anti-tumor, and protective activity, especially for the cardiovascular system and liver.
(...)
CHE downregulated intracellular ROS and increased GSH in the embryos. CHE was also shown to improve the activity of mitochondria and inhibit the occurrence of autophagy. In addition, antioxidant-related genes (SOD1, SOD2, and CAT) and cell pluripotency-related genes (SOX2, OCT4, and NANOG) were upregulated. At the same time, apoptosis-related (Caspase 3) and autophagy-related (LC3B) genes showed a downward trend after supplementation with CHE. These results indicate that CHE improved the development of porcine embryos in vitro by reducing oxidative stress and autophagy levels.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9958645/

Kaempferol alleviates the reduction of developmental competence during aging of porcine oocytes

Zitat

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Furthermore, the mRNA levels of the embryonic pluripotency-related genes Oct4, NANOG, and ITGA5 were significantly increased in blastocysts derived from KAE-treated oocytes (p < .05).

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https://pubmed.ncbi.nlm.nih.gov/31486245/

The effect of quercetin in the maturation media on cumulus-granulosa cells and the developmental competence of bovine oocytes

Zitat

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Relative upregulation of OCT-4, IGF2R and Bcl-2, and downregulation of CHOP was seen in treated oocytes.

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https://pubmed.ncbi.nlm.nih.gov/35809360/

Icaritin enhances mESC self-renewal through upregulating core pluripotency transcription factors mediated by ERα

Zitat

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Icaritin increases mESCs proliferation while maintains their self-renewal capacity in vitro and pluripotency in vivo. This coincides with upregulation of key pluripotency transcription factors OCT4, NANOG, KLF4 and SOX2. The enhancement of mESCs self-renewal is characterized by increased population in S-phase of cell cycle, elevation of Cylin E and Cyclin-dependent kinase 2 (CDK2) and downregulation of p21, p27 and p57.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5238509/

Glucosamine and Silibinin Alter Cartilage Homeostasis through Glycosylation and Cellular Stresses in Human Chondrocyte Cells

Zitat

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We observed an increase in KLF4 mRNA and a decrease in Snail mRNA when TC28a2 cells were treated with glucosamine and silibinin, and these trends were consistent with their proteins.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11084729/

Conserved Biological Processes in Partial Cellular Reprogramming: A Comprehensive Review

Zitat

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Partial or transient cellular reprogramming is defined by the limited induction of pluripotency factors without fully de-differentiating cells into a pluripotent state. Comparing in vitro and in vivo mouse studies, and in vitro studies in humans, supported by visualizations of the interconnections among the data, we show consistent patterns in how such reprogramming modulates key biological processes. Generally, it leads to enhanced chromatin accessibility, upregulation of chromatin modifiers, and improved mitochondrial activity. These changes are accompanied by shifts in stress response programs, such as inflammation, autophagy, and cellular senescence, as well as dysregulation of extracellular matrix pathways. We also underscore the challenges in evaluating complex processes like aging and cellular senescence, given the variability in biomarkers used across studies. Overall, we highlight biological processes consistently influenced by reprogramming while noting that some effects are context-dependent, varying according to cell type, species, sex, and the reprogramming method employed. These insights inform future research and therapeutic applications in aging and regenerative medicine.

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https://www.preprints.org/manuscript/202410.0122/v1

Hallo Prometheus,

hier kann ich nur zustimmen, würde aber noch einen Schritt weiter gehen. Bei Hypo-Methylierungen sind z.B. Vitamin B12/Folat/Vitamin B6 nur die Co-Faktoren zur erneuten Methylierung. Einzelne "Genschalter" können nur vorübergehend aktiviert werden und helfen in vielen Fällen nicht dauerhaft. Bei einer Hyper-Methylierung sind die Therapieansätze evtl. ähnlich zu bewerten. Mit geeigneten Therapiemaßnahmen kann u.a. das Reparaturgen in den Zellen aktiviert werden (z.B. mit BHB), um den Stoffwechsel zu verbessern und die Ergebnisse sind häufig sehr stabil (siehe auch "Lebensenergie", Dr. Strunz 2022).

Viele Grüße und ein schönes Wochenende

Roger

Zitat von Roger im Beitrag #219

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das Reparaturgen

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Hallo,

es geht u.a. um SIRT1: https://www.strunz.com/news/mehr-energie...eres-leben.html .

Viele Grüße und ein schönes Wochenende

Roger

Biohacking To Better Health

People have always been fascinated with immortality. While great gains in medical care have enabled lifespan extension, this has often come with the price of co-existing with chronic diseases associated with aging, such as cardiovascular diseases, cancer, type 2 diabetes mellitus (T2DM), hypertension, and dementias such as Alzheimer’s and Parkinson’s disease.

The true “aim of the game” is to have a long healthspan with negligible senescence. This means the absence of biological aging, such as reducing functional decline in organs and whole-body fitness, delaying loss of reproductive capabilities, and delaying death risk with age progression. What we really want is to extend youth, not aging. In achieving that, we may begin to push the envelope on increasing healthy lifespan.

https://www.zerohedge.com/medical/biohacking-better-health

Expansion of the neocortex and protection from neurodegeneration by in vivo transient reprogramming
https://www.sciencedirect.com/science/ar...iFoo5PI5TcTB9LA

Researchers challenge longstanding theories in cellular reprogramming
https://phys.org/news/2024-11-longstandi...qtBF-S_7Xj6v5Og

Zitat von version2 im Beitrag #215

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#214 Die einfachste Variante dazu:

500mg Curcumin
600mg Tributryn
B12
Multivitamin (optional, empfohlen)

Eine Stunde warten

300mg Apigenin (liposomal)
500mg NAD oder NMN
500mg Tributryn ("another half a gram", 600mg wie vorher wären also wohl auch okay)

Das ganze max. 2 mal täglich. Eine Woche on, dann eine Woche off (Pause).

Quelle: https://i.4pcdn.org/pol/1717465050629414.png

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