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Screening of anti-aging substances and supplement
combinations in world medical journals
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Over the years,
medical journals have confirmed that there are many substances, supplements
and drugs with anti-aging effects and life extension. However, it is very
difficult to really determine which ones can be used for oral treatment. The
following are selected from more than 100 supplements and drugs. During this
period, the filtering principles used are: 1. There are clear targets
and mechanisms of action, and simple observation is not accepted; 2.
The goal is to extend life, excluding the general recognition of "good
for health"; 3. No side effects on various basic diseases; 4.
No allergic precedents have been found; 5. The price is relatively
cheap and easy to buy. Rapamycin is quite special and is still on the list. |
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Rapamycin |
Rapamycin's inhibition of mTORC1 works by
suppressing normal aging and related diseases. The drug combination extended
lifespan by 48%. In addition, combining lithium with rapamycin counteracted
the latter's effects on lipid metabolism. https://www.sciencedirect.com/science/article/pii/S0531556523000876； https://pmc.ncbi.nlm.nih.gov/articles/PMC6814615/
https://www.nature.com/articles/s41598-019-44106-5
Rapamycin is expensive and has significant
side effects, and its analog C15:0 is also expensive. It is recommended to
use alternatives. |
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Isoliquiritigenin |
Isoliquiritigenin activates AMPK and
inhibits mTORC1 signaling, and has good safety. It
is expected to replace rapamycin. https://www.sciencedirect.com/science/article/abs/pii/S0944711322000289?via%3Dihub
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Astaxanthin |
Astaxanthin (ATX) is a carotenoid with significant antioxidant properties[13]. It is a potent activator of Nrf2 and extends the lifespan of mice by 12%. ATX has been shown to reduce interleukin-1β (IL-1β) and interleukin-6 (IL-6) levels, as well as the expression of NF-κB (p65) and i-κ-B-alpha (IκBα) proteins. Its anti-aging effects are thought to be mediated by the activation of the Nrf2/Keap1/NF-κB pathway and subsequent antioxidant activity, as well as anti-immunogenic activity associated with the activation of multiple immune mediators such as interleukins and NF-κB. https://link.springer.com/article/10.1007/s11357-023-01011-0 |
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NAD + |
NAD+ plays a key role in cellular
metabolism and is a co-substrate for enzymes that play key roles in pathways
that alter aging. Therefore, interventions that increase NAD+ may slow
various aspects of the aging trajectory. https://www.sciencedirect.com/science/article/abs/pii/S1471491417301417
https://pmc.ncbi.nlm.nih.gov/articles/PMC7494058/
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Quercetin |
Quercetin has anti-aging and rejuvenating
effects. Maintains the speed of aging and prolongs the youthful morphology of
human primary fibroblasts D+Q is a combination of dasatinib (D) and quercetin
(Q), an anti-aging drug that can remove senescent
cells Pepper Changming + Quercetin removes senescent cells |
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Curcumin + Piperine |
Curcumin has a positive impact on slowing
down the aging process by delaying age-related changes. This compound may
have anti-aging properties by altering the levels of proteins involved in the
aging process, such as sirtuins and AMPK, and inhibiting pro-aging proteins,
such as NF-κB and mTOR. Curcumin bioavailability, and
taking it with piperine can increase bioavailability. |
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Vitamin D |
signaling pathways associated with cell
proliferation and tumorigenicity, and therefore vitamin D3 may have
therapeutic use as an effective, safe, and long-term treatment option for
human UF 1,25D inhibits mTORc1 activity in mouse T cells, and low 25D levels
in humans are associated with reduced expression of mTORc1-inhibitory
tuberous sclerosis complex 1 in CD8+ T cells. In animals with T cell-specific
mTORc1 deficiency. GR upregulation and in vivo therapeutic
effects of 1,25D and 1,25D/GC synergy were abolished. Specific inhibition of
mTORc1 by everolimus increases the efficacy of GC in EAE. 1,25D enhances
GC-mediated effects in vitro and in vivo in a T cell-specific, GR-dependent
manner by inhibiting mTORc1 |
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Vitamin A |
Of the 34 compounds screened in the
high-fidelity validation screen, only VA significantly affected lifespan.
Loss-of-function genetic models suggested that the SKN-1 pathway plays a key
role in VA's lifespan extension. Our study thus provides new insights into
the molecular mechanisms underlying the anti-aging and antioxidant effects of
VA, suggesting that this micronutrient could be used to prevent and/or treat
age-related diseases. Significant associations were observed between retinol
metabolite concentrations and lifespan (Figs. 2 and 3). Specifically, a
10-fold increase in retinol metabolites was causally associated with a 7%
increased odds of longevity (OR 1.07; 95% CI: 1.02-1.13;,
Figure 2). Similarly, significantly higher lifespan years were observed for
genetically predicted higher retinol metabolite levels (lifespan years per
10-fold increase: 0.17; 95% CI: 0.07-0.27;, Figure
3). |
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Lutein |
Lutein can inhibit IL-11: Cardiac
remodeling Lutein inhibits IL-11 expression, thereby attenuating angiotensin
II-induced cardiac remodeling. Overexpression of IL-11 in cardiac tissue
impairs the protective effects of lutein. Cardiac fibrosis Lutein inhibits
AP-1/IL-11 signaling and can reduce angiotensin II-induced cardiac fibrosis.
However, one study found that treatment with LV-IL-11+lutein increased
cardiac fibrosis. Osteoarthritis Lutein treatment inhibits proinflammatory
cytokines such as IL-1β, which may have a bone protective effect. https://pubmed.ncbi.nlm.nih.gov/34077894/
https://www.sciencedirect.com/science/article/abs/pii/S0167494313001143
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Osmanthus herb |
A research team from the University of
Padova Medical School in Italy published a research paper titled
"Targeting senescence induced by age or chemotherapy with a
polyphenol-rich natural extract improves longevity and healthspan in
mice" in the journal Nature Aging. The study found that a sage extract
(HK for short) can significantly extend the lifespan of mice and improve
multiple aging phenotypes in the body. |
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lithium |
The mitogen-activated protein kinase
kinase (MEK) inhibitor trametinib, the mTOR complex 1 (mTORC1) inhibitor
rapamycin, and the glycogen synthase kinase 3 (GSK-3) inhibitor lithium work synergistically
to increase lifespan in fruit flies. Remarkably, the three-drug combination
extended lifespan by 48%. Furthermore, the combination of lithium and
rapamycin counteracted the latter's effects on lipid metabolism. Lithium has been shown to extend lifespan
in both fruit flies and nematodes. Lithium is an exciting frontier in aging
research with its potential anti-aging effects. Its ability to protect
neurons, enhance mitochondrial function, promote autophagy, and reduce
senescent cell load makes it a promising candidate for extending lifespan and
improving brain health, https://www.sciencedirect.com/science/article/abs/pii/S1568163724002149?via%3Dihub
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Alpha-ketoglutarate AKG |
AKG can stimulate the expression of
longevity genes such as FoxO, DAF-16, and SIRT, and inhibit the activation of
the inflammation-related NF-κB signaling pathway, reduce the level of
pro-inflammatory factors, and slow down the rate of inflammatory aging [6].
When the ATP content is too low, it will activate the AMPK signaling pathway,
thereby inhibiting the expression of the mTOR signaling pathway [7]. The
carboxylic acid cycle intermediate AKG can delay aging and extend the
lifespan of Caenorhabditis elegans by about 50% (Figure 2A). In a
concentration-dependent manner, 8 mM AKG produced the maximum lifespan
extension in wild-type N2 worms (Figure 2B). Chin et al. (Chin et al., 2014)
also demonstrated that AKG can not only extend lifespan, but also delay
age-related phenotypes. Retrospective analysis of DNA methylation age in 42 individuals taking Rejuvant? (an alpha-ketoglutarate based formulation) for a mean duration of 7 months. DNAm testing was performed at baseline and at the end of Rejuvant? supplementation treatment. Notably, individuals experienced an average reduction in biological age of 8 years (p-value=6.538x10-12). Furthermore, Rejuvant? supplementation was highly adaptive to individual differences, with the majority of participants experiencing a decrease in biological age. Furthermore, we found that Rejuvant? had additional benefits in individuals with older chronological and physiological age. https://pmc.ncbi.nlm.nih.gov/articles/PMC8660611/ https://pmc.ncbi.nlm.nih.gov/articles/PMC4703346/#b17-bt-24-001
https://www.cell.com/cell-etabolism/fulltext/S1550-4131(20)30417-4?_returnURL=
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CoQ10 |
CoQ10 is an essential component of the
mitochondrial energy transfer system. When CoQ10 levels decrease,
mitochondrial dysfunction increases dramatically and
aging accelerates. In one case, animals that received the supplement had an
average lifespan increase of 11.7% and a maximum lifespan increase of 24%. 1
Based on today’s life expectancy of 78.5 years, this increase is equivalent
to more than nine years of extended human lifespan. However, the benefits of
CoQ10 supplementation are not limited to increased lifespan. Lifelong dietary
supplementation with CoQ10 can even reduce objective markers of aging in
middle-aged animals.
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PCC1 |
PCC1 is the B-type trimer epicatechin
component of the GSE flavonoids and plays an important role in inhibiting
SASP expression at low concentrations and killing senescent cells at high
concentrations (the latter by inducing apoptosis). Drugs that showed preliminary
anti-senescence effects include GSE, quercetin, fisetin, curcumin, and
piperine (Extended Data Fig. 1d, e) Given the efficacy of GSE as a senolytic
inhibitor in reducing the SASP, we next investigated the potential of this natural
product as a senolytic inhibitor to kill senescent cells at higher
concentrations. SA-β-Gal staining showed that
senescent cells were eliminated at a GSE concentration of 0.75 μg ml -1 (Fig.
1a, b). At 3.75 μg ml -1 GSE, the survival rate of senescent cells reached a
plateau of 20% (Fig. 1a, b). This suggests that PCC1 triggers mitochondrial
dysfunction in senescent cells |
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Selenium |
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Taurine |
Taurine deficiency is a driver of aging.
Taurine supplementation slows down key markers of aging, such as increased
DNA damage, telomerase deficiency, impaired mitochondrial function, and
cellular senescence. The median lifespan of taurine-treated mice increased by
10% to 12%, and the life expectancy at 28 months increased by about 18% to
25%. Taurine supplementation slows down key markers of aging, such as
increased DNA damage, telomerase deficiency, impaired mitochondrial function,
and cellular senescence. Taurine inhibits mTOR1. Taurine treatment reduces
mTOR activity and inhibits phosphorylation of ULK1 and ATG13 in MAC-T cells.
Taurine reduced the expression of alcohol-induced TLR4/5/7/9 and its adaptor
protein, MyD88, and the activation of its downstream MAPK (ERK1/2 and P38)
pathway and NF-κB was also lower than that of the alcohol group. In addition,
taurine also reduced the activation of alcohol-induced PI3K/Akt and P53/P21
pathways. Taurine also reduced the expression of pro-inflammatory factors TNF-α,
IL-1β and IL-6 in the liver and serum induced by alcohol. |
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Spermidine |
Spermidine is a bona fide geroprotectant
found naturally in food and is essential for cellular and organismal function
through highly conserved pathways. Seven lines of evidence support its
anti-aging properties: (i) Spermidine levels decrease during aging in most,
but not all, tissues and species studied. (ii) Spermidine supplementation
extends healthspan and lifespan in multiple species. (iii) Epidemiological
data support the view that increasing dietary intake can mitigate, delay, or
prevent age-related deterioration, including cancer, cardiovascular disease,
and cognitive dysfunction. (iv) Metabolic processes within and adjacent to
polyamine pathways are well known, pharmacologically targetable, and highly
conserved across species, allowing for the informed use of models and
development of targeted interventions. (v) Spermidine affects most hallmarks
of aging. (vi) Spermidine appears to be safe in humans. (vii) The
bioavailability of spermidine appears to be fairly good
in mammals, |
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Glycine |
Glycine has been found to extend lifespan
in genetically heterogeneous mice. This simple amino acid has similarly been
shown to extend lifespan in rats and improve health in mammalian models of
age-related diseases. Compelling data suggest that
glycine is a pro-longevity molecule, and the anti-aging drug spermidine
requires Gnmt to upregulate autophagy genes and extend lifespan. Furthermore,
overexpression of Gnmt is sufficient to extend lifespan and reduce methionine
levels. Sarcosine or methylglycine declines with age in multiple species and is able to induce autophagy in vitro and in vivo. In
summary, the available evidence suggests that glycine extends lifespan by
mimicking methionine restriction and activating autophagy. https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.25.1_supplement.528.2 This simple amino acid has been
associated with a variety of benefits in placebo-controlled human studies. In
a group of 74 patients with type 2 diabetes, taking 5000 mg of glycine daily
for three months reduced proinflammatory cytokines and glycated hemoglobin
(HbA1c) (Cruz et al., 2008). In another clinical study involving 60 patients
with metabolic syndrome, taking 15,000 mg of glycine daily for three months
resulted in a decrease in systolic blood pressure (Diaz-Flores et al., 2013).
Two hundred patients with acute ischemic stroke were treated with either 1000
mg/day or 2000 mg/day for five days, and improvements in various stroke
scales were recorded (Gusev et al., 2000). Taking 6000 mg daily for 8 weeks
improved the urine storage system in patients with overactive bladder (Sugaya
et al., 2021), and taking 3000 mg daily for 3 days
reduced fatigue in subjects with sleep restriction (Bannai et al., 2012).
Recently, supplementation with glycine (100 mg/kg/day) and N-acetylcysteine (100 mg/kg/day), two building blocks of
glutathione, has been shown to improve biomarkers associated with several
hallmarks of aging in a group of 24 older adults. As an example
related to chronic inflammatory hallmarks, this supplementation regimen
reduced levels of proinflammatory cytokines in plasma (Kumar et al., 2022a). |
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MAPK metabolic activators |
AMPK activators can all lead to FOXO3
activation. FOXO3-activating compounds are one of the most direct candidates
for extending the healthy lifespan of the elderly. In this work, we review
compounds that activate FOXO3 or affect healthy lifespan or lifespan in a
FOXO3-dependent manner. As a central regulator of multiple metabolic
pathways, AMPK coordinates a vast network of transcription factors in the
body and interacts with multiple signaling pathways involved in lifespan
regulation. https://www.sciencedirect.com/science/article/pii/S1568163722000630
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Oleuropein |
Activating MAPK and extending lifespan |
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Coumarin |
The natural product coumarin can enhance lysosomal function, induce mitophagy and improve mitochondrial function. MIC administration to adult Caenorhabditis elegans for 1-7 days can extend their average lifespan by 40%. Mitochondrial dysfunction is associated with many age-related diseases. Whether in humans or in Caenorhabditis elegans, having healthy mitochondria generally predicts a longer lifespan. Mitochondria, an intracellular autophagy process, aims to remove and recycle damaged mitochondria to maintain normal cell function and metabolism. |
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PQQ |
PQQ acts on the reactive oxygen synthesis/degradation system unique to the cell membrane, generating low levels of reactive oxygen species (ROS) on the cell membrane, and this low level of ROS is the defensive response within the cell. We discovered the mechanism by which "life extension" achieves longevity by exerting important genomic functions and strengthening biological defense. The new food ingredient pyrroloquinoline quinone (PQQ) extends the adult lifespan of nematodes by more than 30%, and the life extension mechanism of PQQ. First time disclosed in the world. Extending lifespan through peroxidase/dual oxidase-mediated ROS signaling https://www.frontiersin.org/journals/aging/articles/10.3389/fragi.2024.1351860/full |
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Sulforaphane |
Activating HSF1 Daily consumption of a certain amount of cruciferous vegetables such as broccoli, cabbage or cauliflower can alleviate diseases such as cancer, inflammation, diabetes and hypertension. Studies have confirmed that the main effect on the above diseases is sulforaphane (SFN), which is generally present in cruciferous vegetables in the form of its precursor glucoraphanin (GLR). When people chew cruciferous vegetables or their extracts, the myrosinase in the vegetables can hydrolyze part of the GLR into SFN; the remaining GLR enters the human body and is hydrolyzed into SFN by intestinal flora such as Escherichia coli, Enterococcus faecalis and Streptococcus spp., and then SFN and its metabolites are mainly excreted through urine. The chemical name of SFN is l-isothiocyanato-4-(methylsulfinyl)butane, which is an isothiocyanate. Studies have shown that SFN is a powerful inducer of phase II detoxification enzymes. Its antioxidant capacity is 20 times that of quercetin and 80 times that of curcumin (CUR), and it has high medicinal potential [1]. SFN is mainly absorbed by the small intestine in the human body. It acts on nuclear factor-erythroid 2-related factor 2 (Nrf2), nuclear factor κB (NF-κB), heat shock factor 1 (HSF1) and epigenetic modification [2], showing pharmacological activities such as anti-tumor [3], anti-inflammatory [4], treatment of diabetes [5] and cardiovascular disease [6]. |
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nutmeg |
NecB activated the AMPK enzyme in differentiated C2C12 cells and affected various signaling pathways in near-mature HDFs, including AMPK, sirtuin, and mTOR signaling pathways [36–39]. The results showed that NecB significantly extended the lifespan of wild-type flies by 42.6% compared to the control group and 11.5% compared to rapamycin (Rap). The extent of lifespan extension achieved in this experimental study is the most effective achieved by other drugs to date. |
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Threonine |
Threonine Threonine can extend female lifespan, especially health. Systems biology approach identifies metabolic characteristics of dietary lifespan and healthspan in different species | Nature Communications Oral methods require special settings, Although there are some small differences between the two fasting methods of one meal a day and calorie restriction, they generally achieve the effect of extending lifespan by activating the serine-glycine-threonine metabolic axis, enhancing detoxification, maintaining molecular synthesis turnover, repair/maintenance, and reducing oxidative stress, and maintaining liver function. |
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Serine |
Serine metabolism in aging and age-related diseases Non-essential amino acids are often overlooked in biomedical research; however, they are an essential component of the metabolism of living organisms. Serine is a metabolite that is indispensable for physiological functions. Serine is a key link connecting glycolysis to one-carbon and lipid metabolism and to pyruvate and glutathione synthesis. Interestingly, accumulating evidence suggests that serine metabolism may influence the aging process and that supplementation with serine may help prevent aging and age-related diseases. This review synthesizes recent insights into the regulation of serine metabolism during aging and its potential to promote healthy lifespan and mitigate a range of age-related diseases. |
Citrulline |
Citrulline is a potent inhibitor of mammalian target of rapamycin (mTOR) activation in macrophages and modulates the mTOR-hypoxia-inducible factor 1α-glycolysis signaling pathway to counteract inflammation and aging. Citrulline supplementation is highlighted as a promising therapeutic intervention to counteract aging-related changes. |
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Zingerone A |
Both D+Q and zingerone A had significant effects on suppressing the senescence-associated secretory phenotype (SASP). Zingerone A selectively promoted the death of senescent cells, but had no effect on non-senescent cells. |
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Fisetin |
The flavonoid fisetin inhibits LPS-induced inflammation and endotoxin shock through the interaction between GSK-3β/β-catenin and NF-κB signaling pathways, and fisetin inhibits the mTOR pathway. mTOR accelerates aging and can effectively remove senescent cells. |
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Glucosamine + Chondroitin Sulfate |
Oral supplementation with chondroitin sulfate has demonstrated high tolerability in humans, improved pharmacokinetics, a positive correlation with healthy human lifespan, and efficacy in slowing age-related diseases in randomized clinical trials Endogenous chondroitin extends lifespan by inhibiting VHA-7-mediated tubular lysosome formation https://www.nature.com/articles/s41598-024-80242-3 |
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Omega-3 |
Omega-3 polyunsaturated fatty acids inhibit IL11 https://pmc.ncbi.nlm.nih.gov/articles/PMC8416141/ https://pmc.ncbi.nlm.nih.gov/articles/PMC5032683/ |
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Rutin |
Rutin exerts its effect on the AkT/PI3K/mTOR pathway by regulating the expression of several key proteins (including AkT, PTEN, ERK, etc.). Senolytics or Senomorphics drugs targeting senescent cells have the potential to alleviate the vast majority of age-related diseases, including but not limited to neurodegenerative diseases, cardiovascular diseases, metabolic diseases, musculoskeletal diseases, liver diseases, lung diseases and kidney diseases. However, the main challenge in developing new Senomorphics drugs is the lack of anti-aging agents with good safety. https://pubmed.ncbi.nlm.nih.gov/33555034/ https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1111/bph.15410 |
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Resveratrol |
Some of the beneficial effects of resveratrol may be attributed to
the regulation of S6K1 activity. Resveratrol
(3,4′,5-trihydroxy-trans-stilbene) is the most extensively studied stilbene
compound and is found in grape skins, berries, peanuts, and some medicinal
plants [3], [4], [6]. Hundreds of studies have shown that resveratrol has a
variety of biological and pharmacological effects, including antioxidant,
anti-inflammatory, carcinogenic, and antidiabetic effects, and plays a key
role in human health and disease [7], [8], [9], [10], [11], [12], [13].
However, a potential problem with resveratrol is that its bioavailability is
very low, which may reduce its bioavailability. Resveratrol may exert its anti-aging effects by inhibiting S6K and
activating sirtuins, and some researchers have suggested using pterostilbene
as an alternative. Pterostilbene (along with other CR mimetics and
calorie-restricted diets) has been found to naturally inhibit the mTOR
pathway. 24 This reduction in mTOR provides a powerful way to modulate cell
growth and metabolism and combat some of the major factors associated with
aging and disease. Pterostilbene modulates the activation of key anti-aging molecules called silent information regulators (SIRs) or sirtuins. Sirtuins play a role in regulating multiple cellular pathways involved in gene expression, aging, DNA repair, metabolism, and apoptosis. 32-34 Studies have also examined the important role sirtuins play in maintaining telomere length. |
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Metformin |
Biguanides stimulate the biosynthesis of ether esters to extend
the lifespan of organisms. However, when the ether ester biosynthesis
machinery is missing, dietary restriction, rapamycin target (TOR) inhibition,
and mitochondrial electron transport chain inhibition will occur, inhibiting
the extension of lifespan. Ether esters are essential for "longevity" - downstream
of the conserved transcription factor skn-1/Nrf, ether esters are required
for the activation of longevity promotion and metabolic stress defense. Lack of ether ester biosynthesis, isp-1, raga-1 and eat-2
mutants have inhibited the extension of lifespan Metformin stimulates the body to produce more ether lipids (the main component of cell membranes), and increased ether lipids help to extend lifespan (healthy aging) |
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Betaine |
Three anti-aging drugs (metformin, quercetin, and minocycline) were used to explore the metabolic effects of aging interventions. The expression of betaine was significantly increased under the treatment of the three anti-aging drugs. It was mainly through pathways related to the forkhead box transcription factor (FoxO) signaling pathway, the p38 mitogen-activated protein kinase (MAPK) signaling pathway, autophagy, longevity regulation pathway, and rapamycin target (mTOR) signaling pathway |
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Licholic acid |
Lithocholic acid (LCA) was one of the metabolites that alone recapitulated the effects of CR in mice. These effects included activation of AMP-activated protein kinase (AMPK), enhanced muscle regeneration, and restoration of grip strength and running ability. LCA also activated AMPK and induced lifespan- and healthspan-extending effects in C. elegans and D. melanogaster. As C. elegans and D. melanogaster are unable to synthesize LCA, these results suggest that these animals are able to transmit the signaling effects of LCA once administered. Knockout of AMPK abolished the LCA-induced phenotypes in all three animal models. In summary, we determined that administration of the CR-mediated upregulated metabolite LCA alone can confer anti-aging benefits to metazoans in an AMPK-dependent manner. |
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Berberine |
BBR extended the replicative lifespan, improved morphology, and
enhanced regression markers of replicative senescence in human fetal lung
diploid fibroblasts (2BS and WI38). BBR also rescued senescent cells from
late population doublings (PD). Moreover, the rate of senescence-associated
β-galactosidase (SA-β-gal)-positive cells in late PD cells grown in medium
containing BBR was about 72% lower than that of control cells, and their
morphology resembled that of young cells. Mechanistically, BBR improved cell
growth and proliferation by promoting the entry of the cell cycle from G?0 or
G?1 phase into the S/G?2?-M phase. Most importantly,
BBR extended the lifespan of mice treated with chemotherapy and naturally
aged mice by about 52% and about 16.49%, respectively. The remaining lifespan
of naturally aged mice was extended by 80%, from 85.5 days to 154 days. Oral
administration of BBR to mice significantly improved health span, hair
density, and behavioral activity. Therefore, BBR may be an ideal candidate
for the development of anti-aging drugs. Berberine, like the anti-diabetic drug metformin, is an activator of an enzyme (AMPK) that is involved in some of the beneficial anti-aging effects of caloric restriction. Resveratrol and pterostilbene reduce the risk of inflammation, heart disease, cancer, and neurodegenerative diseases, in addition to protecting the integrity of the genome by activating enzymes called "sirtuins." Nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) supplements are effective in increasing levels of nicotinamide adenine dinucleotide (NAD), which decline with age. Some of these supplements can extend lifespan in a variety of organisms (yeast, worms, flies) and experimental animals (mice, rats), but there is currently no evidence that they have such an effect in humans. |
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AP2A1 protein inhibition |
Curcumin, resveratrol, quercetin, and PCC1 can inhibit the expression or activity of AP2A1 protein. In addition, some studies have found that certain microRNAs can target AP2A1 mRNA, thereby inhibiting the translation of AP2A1 protein. https://pmc.ncbi.nlm.nih.gov/articles/PMC8806629/ https://www.e3s-conferences.org/articles/e3sconf/pdf/2024/30/e3sconf_interconnects2024_04002.pdf |
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Rilmenidine |
Rilmenidine? This is a drug for treating high blood pressure, but long-term use can effectively extend lifespan. ? I1-imidazoline receptor agonist and prescription drug for treating high blood pressure. We then showed that treating C. elegans with limenidine in young and old age can extend lifespan, and that limenidine extends lifespan and healthspan of C. elegans via the glycoprotein I1-imidazoline receptor (do not use if you have low blood pressure) https://pmc.ncbi.nlm.nih.gov/articles/PMC9924948/ https://onlinelibrary.wiley.com/doi/10.1111/acel.13774 |
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Tyrosine inhibition |
Dietary tyrosine deprivation reduces internal tyrosine levels and fecundity, affects AA sensing mechanisms, and extends lifespan. |
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Rough information |
1 Restricting the intake of isoleucine and methionine in the diet
can significantly improve the metabolic health of mice and prolong the
healthy life span. SGLT2 inhibition eliminates senescent cells and alleviates
pathological aging 2 Healthy lifestyle and diet; regular fasting 5:3, 8:16;
appropriate exercise Reducing dietary intake can not only reduce the accumulation of
fat in adipose tissue, but also affect cell signaling pathways, thereby
prolonging life and inhibiting the aging process. The beneficial effects of
DR may be related to the reduction in protein intake; restricting the intake
of branched-chain amino acids will increase the life span and healthy life
span of rodents/ 5 Timely treatment of underlying diseases 6 TERT activator compound (TAC), which can enhance TERT
transcription in adult somatic cells of humans and mice, restore it to the
physiological expression level in young cells, promote telomere synthesis,
and reduce DNA damage signals at telomeres, thereby reversing cell aging. 7 Inject young blood 8 Manipulate the gene circuit that controls aging, chemically
induced reprogramming to reverse cell aging, 9 Can a certain technical means slow down the working speed of the
"translator" (genetic transcription) (key enzyme RNA polymerase II
for "fine-tuning"), delay aging, Gene editing of the key cell enzyme "RNA polymerase II"
can slow down the speed of information translation 10 Inject interleukin antibodies to inhibit interleukin 11 Inhibiting IL-11 signaling can extend the healthy lifespan and
lifespan of mammals 11 Clean up senescent cells regularly once a month Clearing senescent cells can delay aging 12 "Gene-encoded resilience" is identified as the "key factor" for longevity |
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