Topical Rapamycin
Introduction:
A drug called topical rapamycin is employed in a number of dermatological procedures. It originates from the immunosuppressive qualities of the naturally occurring substance known as rapamycin, which was first found in the soil of Easter Island.
It has been demonstrated that rapamycin lowers the body's overall senescent cell count. The term "cellular senescence" describes a condition in which cells no longer have the capacity to divide and proliferate and instead experience a persistent and irreversible growth stop.
Senescent cells build up with ageing and have a role in a number of age-related illnesses and ailments. Will discuss more about Rapamycin below.
"Rapamycin reduces the total amount of senescent cells”
• It has been revealed that rapamycin, a drug produced from the substance first identified on Easter Island, has the capacity to lessen the overall amount of senescent cells in the body. Age-related cell accumulation of senescent cells, which are cells that have reached an irreversible growth halt.
• Rapamycin causes a process known as autophagy, which includes the recycling and destruction of damaged cellular components, by blocking a protein known as mTOR (mammalian target of rapamycin). Senescent cells and cell waste are removed via autophagy.
• Rapamycin therapy has been shown in several trials to reduce the number of senescent cells in a variety of organs, including the skin, liver, and adipose tissue. In several animal models, this decrease in senescent cells has been linked to a number of positive outcomes, including better tissue function, higher regenerative ability, and prolonged life.
• Studies on anti-aging and age-related diseases are increasingly focusing on the treatment of senescent cells. Senescent cell burden reduction is thought to offer therapeutic promise for a number of illnesses, including cancer, neurological disorders, and cardiovascular ailments.
• To completely comprehend the effects of rapamycin, including ideal dose and possible adverse effects, further study is still required. The effectiveness and safety of rapamycin and other senolytic treatments in humans are now being studied in clinical studies.
• The medication rapamycin is a member of the group of substances known as mTOR inhibitors. A protein kinase known as mTOR (mechanistic target of rapamycin) is essential for cell growth, metabolism, and ageing.
• Rapamycin has been shown to have potential anti-aging properties and has been found to alter a number of cellular processes via blocking mTOR.
Introduction:
A drug called topical rapamycin is employed in a number of dermatological procedures. It originates from the immunosuppressive qualities of the naturally occurring substance known as rapamycin, which was first found in the soil of Easter Island.
It has been demonstrated that rapamycin lowers the body's overall senescent cell count. The term "cellular senescence" describes a condition in which cells no longer have the capacity to divide and proliferate and instead experience a persistent and irreversible growth stop.
Senescent cells build up with ageing and have a role in a number of age-related illnesses and ailments. Will discuss more about Rapamycin below.
"Rapamycin reduces the total amount of senescent cells”
• It has been revealed that rapamycin, a drug produced from the substance first identified on Easter Island, has the capacity to lessen the overall amount of senescent cells in the body. Age-related cell accumulation of senescent cells, which are cells that have reached an irreversible growth halt.
• Rapamycin causes a process known as autophagy, which includes the recycling and destruction of damaged cellular components, by blocking a protein known as mTOR (mammalian target of rapamycin). Senescent cells and cell waste are removed via autophagy.
• Rapamycin therapy has been shown in several trials to reduce the number of senescent cells in a variety of organs, including the skin, liver, and adipose tissue. In several animal models, this decrease in senescent cells has been linked to a number of positive outcomes, including better tissue function, higher regenerative ability, and prolonged life.
• Studies on anti-aging and age-related diseases are increasingly focusing on the treatment of senescent cells. Senescent cell burden reduction is thought to offer therapeutic promise for a number of illnesses, including cancer, neurological disorders, and cardiovascular ailments.
• To completely comprehend the effects of rapamycin, including ideal dose and possible adverse effects, further study is still required. The effectiveness and safety of rapamycin and other senolytic treatments in humans are now being studied in clinical studies.
• The medication rapamycin is a member of the group of substances known as mTOR inhibitors. A protein kinase known as mTOR (mechanistic target of rapamycin) is essential for cell growth, metabolism, and ageing.
• Rapamycin has been shown to have potential anti-aging properties and has been found to alter a number of cellular processes via blocking mTOR.
• Numerous studies have shown that rapamycin therapy can lessen the formation of senescent cells in both animal and human cells. It is believed that rapamycin's senolytic effects are caused by a number of different pathways. Senescent cells can be selectively eliminated from the body by rapamycin by inducing apoptosis (programmed cell death) in such cells. Rapamycin can also improve the immune system's capacity to eliminate senescent cells.
• Senescent cells can contribute to tissue malfunction and encourage inflammation, which are important causes of age-related disorders, therefore reducing their number is a desired goal. Rapamycin may have the ability to lengthen life expectancy and postpone the onset of age-related diseases by eliminating or decreasing senescent cells.
• It's important to remember that the prescription medicine rapamycin is mostly utilised as an immunosuppressant to avoid organ transplant rejection and in the treatment of certain malignancies.
• Even though it has demonstrated promise as an anti-aging strategy, more study is still required to properly comprehend its long-term benefits, ideal dose regimes, and potential adverse effects in the context of ageing.
More information:
• Mechanism of action: Rapamycin works by inhibiting the protein kinase mTOR, which is involved in cellular activities such protein synthesis, cell proliferation, and autophagy. Rapamycin slows or stops some biological processes, such as the buildup of senescent cells, by blocking mTOR.
• Senescent cell clearance: Rapamycin has been demonstrated to improve senescent cell clearance through a number of ways. Senescent cells can experience apoptosis, or cell death, which enables the body to get rid of them. Rapamycin also activates the immune system's immunosurveillance mechanism, which helps it identify and destroy senescent cells.
• Benefits for healthspan: Removing or decreasing senescent cells has been associated with a number of healthspan advantages. Chronic inflammation, tissue malfunction, and age-related illnesses including cancer, cardiovascular disease, and neurological disorders are all linked to senescent cells. Rapamycin may assist in alleviating certain age-related diseases and enhancing general health and longevity by lowering the load of senescent cells.
• Studies on animals: Rapamycin has showed encouraging effects in reducing senescent cells. It has been shown that rapamycin therapy in mice reduces the development of senescent cells in a variety of organs, including the liver, adipose tissue, and skeletal muscle. Additionally, these research have demonstrated improved ageing characteristics and lengthened longevity in certain mice models.
• Studies on humans: Although rapamycin has been the subject of substantial research in animals, nothing is known about how it affects senescent cells in people. There are now some clinical trials looking at how rapamycin affects ageing and age-related
• Senescent cells can contribute to tissue malfunction and encourage inflammation, which are important causes of age-related disorders, therefore reducing their number is a desired goal. Rapamycin may have the ability to lengthen life expectancy and postpone the onset of age-related diseases by eliminating or decreasing senescent cells.
• It's important to remember that the prescription medicine rapamycin is mostly utilised as an immunosuppressant to avoid organ transplant rejection and in the treatment of certain malignancies.
• Even though it has demonstrated promise as an anti-aging strategy, more study is still required to properly comprehend its long-term benefits, ideal dose regimes, and potential adverse effects in the context of ageing.
More information:
• Mechanism of action: Rapamycin works by inhibiting the protein kinase mTOR, which is involved in cellular activities such protein synthesis, cell proliferation, and autophagy. Rapamycin slows or stops some biological processes, such as the buildup of senescent cells, by blocking mTOR.
• Senescent cell clearance: Rapamycin has been demonstrated to improve senescent cell clearance through a number of ways. Senescent cells can experience apoptosis, or cell death, which enables the body to get rid of them. Rapamycin also activates the immune system's immunosurveillance mechanism, which helps it identify and destroy senescent cells.
• Benefits for healthspan: Removing or decreasing senescent cells has been associated with a number of healthspan advantages. Chronic inflammation, tissue malfunction, and age-related illnesses including cancer, cardiovascular disease, and neurological disorders are all linked to senescent cells. Rapamycin may assist in alleviating certain age-related diseases and enhancing general health and longevity by lowering the load of senescent cells.
• Studies on animals: Rapamycin has showed encouraging effects in reducing senescent cells. It has been shown that rapamycin therapy in mice reduces the development of senescent cells in a variety of organs, including the liver, adipose tissue, and skeletal muscle. Additionally, these research have demonstrated improved ageing characteristics and lengthened longevity in certain mice models.
• Studies on humans: Although rapamycin has been the subject of substantial research in animals, nothing is known about how it affects senescent cells in people. There are now some clinical trials looking at how rapamycin affects ageing and age-related
disorders. In these studies, rapamycin and its analogues will be tested on humans to determine their safety, effectiveness, and any possible adverse effects.
• Considerations and restrictions: Rapamycin is a prescription medication with possible adverse effects, and research on its long-term impact on ageing and human health is ongoing. Research is still being conducted on the best dose, length of therapy, and possible side effects of rapamycin for anti-aging objectives.
Conclusion:
• In conclusion, the claim that rapamycin lowers the overall number of senescent cells is supported by the available data. Animal preclinical investigations have shown that rapamycin therapy can reduce the formation of senescent cells in a variety of organs.
• Senescent cells may undergo apoptosis due to rapamycin, which also makes the immune system more effective in eliminating them. To completely comprehend the effects of rapamycin on senescent cells in people and to establish the ideal dosage schedules and potential adverse effects connected with its usage for this purpose, more study is necessary.
• Rapamycin should thus be used cautiously and in accordance with medical advice even if it has promise as a senolytic drug.
Evidence based articles and links:
• “Topical rapamycin reduces markers of senescence and aging in human skin: an exploratory, prospective, randomized trial”: https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC6925069/
• “Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2‐independent mechanism”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5418203/
• “The mTOR inhibitor Rapamycin protects from premature cellular senescence early after experimental kidney transplantation”: https://journals.plos.org/plosone/article? id=10.1371/journal.pone.0266319
• “Effect of rapamycin on aging and age-related diseases—past and future”: https:// link.springer.com/article/10.1007/s11357-020-00274-1
• “Progressive slowdown/prevention of cellular senescence by CD9-targeted delivery of rapamycin using lactose-wrapped calcium carbonate nanoparticles”: https:// www.nature.com/articles/srep43299
• “Targeting senescent cells: approaches, opportunities, challenges”: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC6949083/ #:~:text=SUPPRESS%20SENESCENT%20CELLS-,Senolytics,in%20senescent%20cel ls%20%5B16%5D.
• “Cell senescence, rapamycin and hyperfunction theory of aging”: https:// www.tandfonline.com/doi/full/10.1080/15384101.2022.2054636
• Considerations and restrictions: Rapamycin is a prescription medication with possible adverse effects, and research on its long-term impact on ageing and human health is ongoing. Research is still being conducted on the best dose, length of therapy, and possible side effects of rapamycin for anti-aging objectives.
Conclusion:
• In conclusion, the claim that rapamycin lowers the overall number of senescent cells is supported by the available data. Animal preclinical investigations have shown that rapamycin therapy can reduce the formation of senescent cells in a variety of organs.
• Senescent cells may undergo apoptosis due to rapamycin, which also makes the immune system more effective in eliminating them. To completely comprehend the effects of rapamycin on senescent cells in people and to establish the ideal dosage schedules and potential adverse effects connected with its usage for this purpose, more study is necessary.
• Rapamycin should thus be used cautiously and in accordance with medical advice even if it has promise as a senolytic drug.
Evidence based articles and links:
• “Topical rapamycin reduces markers of senescence and aging in human skin: an exploratory, prospective, randomized trial”: https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC6925069/
• “Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2‐independent mechanism”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5418203/
• “The mTOR inhibitor Rapamycin protects from premature cellular senescence early after experimental kidney transplantation”: https://journals.plos.org/plosone/article? id=10.1371/journal.pone.0266319
• “Effect of rapamycin on aging and age-related diseases—past and future”: https:// link.springer.com/article/10.1007/s11357-020-00274-1
• “Progressive slowdown/prevention of cellular senescence by CD9-targeted delivery of rapamycin using lactose-wrapped calcium carbonate nanoparticles”: https:// www.nature.com/articles/srep43299
• “Targeting senescent cells: approaches, opportunities, challenges”: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC6949083/ #:~:text=SUPPRESS%20SENESCENT%20CELLS-,Senolytics,in%20senescent%20cel ls%20%5B16%5D.
• “Cell senescence, rapamycin and hyperfunction theory of aging”: https:// www.tandfonline.com/doi/full/10.1080/15384101.2022.2054636
Longevity Genes
List of genes responsible for Longevity:
The complicated attribute of longevity is impacted by a number of genetic, environmental, and lifestyle variables. Even while research into the genetic causes of longevity is ongoing, it's crucial to remember that no one gene can be entirely to blame for determining lifetime.
However, certain genes have been linked to long life and are thought to contribute to the ageing process. Based on research, the following genes have been associated with long life:
FOXO3: This gene has been linked to remarkable human lifespan and is involved in controlling the insulin/insulin-like growth factor (IGF) signalling pathway. Source: “FOXO3 and Exceptional Longevity: Insights From Hydra to Humans”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7295567/
SIRT1: This gene is a member of the sirtuin gene family, which plays a variety of roles in cellular functions such DNA repair, metabolism, and stress response. SIRT1 has been associated with increased longevity in a number of model species. Source: “The Role of SIRT1 on DNA Damage Response and Epigenetic Alterations in Cancer”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651129/
MTOR: The protein kinase known as the mammalian target of rapamycin (mTOR) controls cellular development, metabolism, and ageing. Numerous creatures have showed longer lifespans when mTOR signalling is inhibited. Source: “Mammalian Target of Rapamycin”: https://www.sciencedirect.com/topics/neuroscience/mammalian-target-of-rapamycin
APOC3: Variants of the APOC3 gene have been linked to prolonged longevity and a decreased risk of cardiovascular illnesses. Source: “ApoC-III: a potent modulator of hypertriglyceridemia and cardiovascular disease”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524519/
CETP: The cholesteryl ester transfer protein (CETP) gene has genetic variants that have been linked to increased lifespan and a decreased chance of developing age-related disorders. Source: “Cholesteryl Ester Transfer Protein (CETP) Genotype and Reduced CETP Levels Associated With Decreased Prevalence of Hypertension”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878255/
TERT: Telomeres, which are protective structures at the ends of chromosomes, are maintained by telomerase reverse transcriptase (TERT). Telomere length and longevity variations have been linked to variations in the TERT gene. Source: “Telomeres and Telomere Length: A General Overview”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139734/
APOB: Apolipoprotein B (APOB) gene variations have been associated with remarkable lifespan and a lower risk of cardiovascular illnesses. Source: “Apolipoprotein B and Cardiovascular Disease: Biomarker and Potential Therapeutic Target”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8540246/
KLOTHO: A protein that has been linked to ageing and lifespan is encoded by the KLOTHO gene. KLOTHO gene variations have been linked to increased longevity and cognitive performance. Source: “Klotho and aging”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743784/
NRF2: The nuclear factor erythroid 2-related factor 2 (NRF2) gene controls cellular stress defences and antioxidant responses. In model organisms, activation of NRF2 has been associated with longer life. Source: “The KEAP1-NRF2 System in Healthy Aging and Longevity”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750203/#:~:text=The%20KEAP1%2DNRF2%20activity%20and%20longevity.&text=In%20experimental%20models%2C%20mild%20activation,tolerance%2C%20accelerates%20the%20aging%20process.
PON1: The paraoxonase 1 (PON1) gene encodes an enzyme that is involved in lipid metabolism and oxidative stress defence. Age-related illness risk has been shown to be lower and lifespan has been linked to variations in the PON1 gene. Source: “PON1 is a longevity gene: results of a meta-analysis”: https://pubmed.ncbi.nlm.nih.gov/19376276/#:~:text=Patients%20carrying%20PON1%20codon%20192,represented%20in%20long%2Dliving%20individuals.
List of genes responsible for Longevity:
The complicated attribute of longevity is impacted by a number of genetic, environmental, and lifestyle variables. Even while research into the genetic causes of longevity is ongoing, it's crucial to remember that no one gene can be entirely to blame for determining lifetime.
However, certain genes have been linked to long life and are thought to contribute to the ageing process. Based on research, the following genes have been associated with long life:
FOXO3: This gene has been linked to remarkable human lifespan and is involved in controlling the insulin/insulin-like growth factor (IGF) signalling pathway. Source: “FOXO3 and Exceptional Longevity: Insights From Hydra to Humans”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7295567/
SIRT1: This gene is a member of the sirtuin gene family, which plays a variety of roles in cellular functions such DNA repair, metabolism, and stress response. SIRT1 has been associated with increased longevity in a number of model species. Source: “The Role of SIRT1 on DNA Damage Response and Epigenetic Alterations in Cancer”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651129/
MTOR: The protein kinase known as the mammalian target of rapamycin (mTOR) controls cellular development, metabolism, and ageing. Numerous creatures have showed longer lifespans when mTOR signalling is inhibited. Source: “Mammalian Target of Rapamycin”: https://www.sciencedirect.com/topics/neuroscience/mammalian-target-of-rapamycin
APOC3: Variants of the APOC3 gene have been linked to prolonged longevity and a decreased risk of cardiovascular illnesses. Source: “ApoC-III: a potent modulator of hypertriglyceridemia and cardiovascular disease”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524519/
CETP: The cholesteryl ester transfer protein (CETP) gene has genetic variants that have been linked to increased lifespan and a decreased chance of developing age-related disorders. Source: “Cholesteryl Ester Transfer Protein (CETP) Genotype and Reduced CETP Levels Associated With Decreased Prevalence of Hypertension”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878255/
TERT: Telomeres, which are protective structures at the ends of chromosomes, are maintained by telomerase reverse transcriptase (TERT). Telomere length and longevity variations have been linked to variations in the TERT gene. Source: “Telomeres and Telomere Length: A General Overview”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139734/
APOB: Apolipoprotein B (APOB) gene variations have been associated with remarkable lifespan and a lower risk of cardiovascular illnesses. Source: “Apolipoprotein B and Cardiovascular Disease: Biomarker and Potential Therapeutic Target”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8540246/
KLOTHO: A protein that has been linked to ageing and lifespan is encoded by the KLOTHO gene. KLOTHO gene variations have been linked to increased longevity and cognitive performance. Source: “Klotho and aging”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743784/
NRF2: The nuclear factor erythroid 2-related factor 2 (NRF2) gene controls cellular stress defences and antioxidant responses. In model organisms, activation of NRF2 has been associated with longer life. Source: “The KEAP1-NRF2 System in Healthy Aging and Longevity”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750203/#:~:text=The%20KEAP1%2DNRF2%20activity%20and%20longevity.&text=In%20experimental%20models%2C%20mild%20activation,tolerance%2C%20accelerates%20the%20aging%20process.
PON1: The paraoxonase 1 (PON1) gene encodes an enzyme that is involved in lipid metabolism and oxidative stress defence. Age-related illness risk has been shown to be lower and lifespan has been linked to variations in the PON1 gene. Source: “PON1 is a longevity gene: results of a meta-analysis”: https://pubmed.ncbi.nlm.nih.gov/19376276/#:~:text=Patients%20carrying%20PON1%20codon%20192,represented%20in%20long%2Dliving%20individuals.
PubMed Central (PMC)
FOXO3 and Exceptional Longevity: Insights From Hydra to Humans
Aging is a complex, multifactorial process with significant plasticity. While several biological pathways appear to influence aging, few genes have been identified that are both evolutionarily conserved and have a strong impact on aging and age-related ...
GSTM1: The glutathione S-transferase mu 1 (GSTM1) gene results in the production of an enzyme that aids in the detoxification of a number of substances. Increased longevity and better health outcomes have been linked to certain GSTM1 gene variants. Source: “GSTM1”: http://www.cancerindex.org/geneweb/GSTM1.htm#:~:text=GSTM1%20is%20a%20glutathione%20S,a%20range%20of%20different%20cancers.
HSPA1A/HSPA1B: These genes are members of the heat shock protein (HSP) family and are involved in the regulation of protein quality and the response of cells to stress. Longevity and enhanced stress tolerance have been related to variations in the HSPA1A and HSPA1B genes. Source: “Anti-Inflammatory Heat Shock Protein 70 Genes are Positively Associated with Human Survival”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631775/
PINK1: PTEN-induced putative kinase 1 (PINK1) gene mutations have been linked to Parkinson's disease. A longer lifespan and resistance to cellular stress have also been associated with certain PINK1 gene variants. Source: “PINK1 signaling in mitochondrial homeostasis and in aging (Review)”: https://www.spandidos-publications.com/10.3892/ijmm.2016.2827
BPIFB4: The innate immune system is regulated by the gene BPI fold-containing family B member 4 (BPIFB4). Alterations in the BPIFB4 gene have been linked to a longer life expectancy and a lower chance of developing age-related disorders. Source: “The longevity-associated BPIFB4 gene supports cardiac function and vascularization in aging cardiomyopathy”: https://pubmed.ncbi.nlm.nih.gov/36635236/
TP53: The TP53 gene produces the tumour protein p53, which is essential for DNA repair, controlling the cell cycle, and causing apoptosis. Longevity and a lower chance of developing cancer have been associated with certain TP53 gene variants. Source: “The Regulation of Aging and Longevity”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135645/
Should they all be applied at once? Or maybe it depends on the individual?
It is uncommon to employ the genes linked to long life as a single package or treatment. Instead, they behave as possible predictors of characteristics that could support lifespan. These genes can have a complicated and variable impact on longevity depending on the person, their genetic composition, and their environment.
It's critical to remember that genetics only accounts for a small portion of lifespan. Diet, exercise, stress management, and environmental influences are all important lifestyle aspects.
It is also difficult to separate the influence of specific genes in a complex characteristic like lifespan since the interaction between genes and environment is a dynamic process.
The majority of the present knowledge on genes linked to long life is derived from observational research and genetic association studies, which offer correlations rather than causes.
As a result, it is not advised to utilise genetic data for lifespan as a firm prescription or treatment strategy. Instead, it is generally agreed that the ideal method for maintaining lifespan and wellbeing is a complete approach that includes a healthy lifestyle, frequent medical checkups, and proactive treatment of risk factors.
Evidence based articles and links:
“Genetics of extreme human longevity to guide drug discovery for healthy ageing”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7912776/
“The Genetics of Aging”: https://www.annualreviews.org/doi/10.1146/annurev.genom.2.1.435
HSPA1A/HSPA1B: These genes are members of the heat shock protein (HSP) family and are involved in the regulation of protein quality and the response of cells to stress. Longevity and enhanced stress tolerance have been related to variations in the HSPA1A and HSPA1B genes. Source: “Anti-Inflammatory Heat Shock Protein 70 Genes are Positively Associated with Human Survival”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631775/
PINK1: PTEN-induced putative kinase 1 (PINK1) gene mutations have been linked to Parkinson's disease. A longer lifespan and resistance to cellular stress have also been associated with certain PINK1 gene variants. Source: “PINK1 signaling in mitochondrial homeostasis and in aging (Review)”: https://www.spandidos-publications.com/10.3892/ijmm.2016.2827
BPIFB4: The innate immune system is regulated by the gene BPI fold-containing family B member 4 (BPIFB4). Alterations in the BPIFB4 gene have been linked to a longer life expectancy and a lower chance of developing age-related disorders. Source: “The longevity-associated BPIFB4 gene supports cardiac function and vascularization in aging cardiomyopathy”: https://pubmed.ncbi.nlm.nih.gov/36635236/
TP53: The TP53 gene produces the tumour protein p53, which is essential for DNA repair, controlling the cell cycle, and causing apoptosis. Longevity and a lower chance of developing cancer have been associated with certain TP53 gene variants. Source: “The Regulation of Aging and Longevity”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135645/
Should they all be applied at once? Or maybe it depends on the individual?
It is uncommon to employ the genes linked to long life as a single package or treatment. Instead, they behave as possible predictors of characteristics that could support lifespan. These genes can have a complicated and variable impact on longevity depending on the person, their genetic composition, and their environment.
It's critical to remember that genetics only accounts for a small portion of lifespan. Diet, exercise, stress management, and environmental influences are all important lifestyle aspects.
It is also difficult to separate the influence of specific genes in a complex characteristic like lifespan since the interaction between genes and environment is a dynamic process.
The majority of the present knowledge on genes linked to long life is derived from observational research and genetic association studies, which offer correlations rather than causes.
As a result, it is not advised to utilise genetic data for lifespan as a firm prescription or treatment strategy. Instead, it is generally agreed that the ideal method for maintaining lifespan and wellbeing is a complete approach that includes a healthy lifestyle, frequent medical checkups, and proactive treatment of risk factors.
Evidence based articles and links:
“Genetics of extreme human longevity to guide drug discovery for healthy ageing”: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7912776/
“The Genetics of Aging”: https://www.annualreviews.org/doi/10.1146/annurev.genom.2.1.435
https://www.newscientist.com/article/mg25834382-900-ageing-is-inevitable-but-we-may-soon-treat-it-like-any-other-disease/
#longevity
#longevityintime
#antiaging
#invest
#longevity
#longevityintime
#antiaging
#invest
New Scientist
Ageing is inevitable, but we may soon treat it like any other disease
Getting older is a fact of life, but there are promising signs that we may be able to intervene to slow – and possibly even stop – the molecular processes that lead to numerous age-related conditions
More news regarding quercetin + Dasatinib.
https://www.lifespan.io/news/benefits-of-dasatinib-and-quercetin-treatment-in-monkeys/
https://www.lifespan.io/news/benefits-of-dasatinib-and-quercetin-treatment-in-monkeys/
www.lifespan.io
Benefits of Dasatinib and Quercetin Treatment in Monkeys
In one of the first studies of its kind, the popular senolytic combination, administered systematically for six months, produced several health benefits in these animals. Some effects were augmented by caloric restriction [1]. Coup de grâce for […]
Have you heard about fascinating Bryan Johnson who is reversing aging, for 2M$ per year with the help of 30 doctors, incl. brilliant Oliver Zolman who advised us for some time?
https://youtu.be/aj3bQa6gcOg
We do the same, but with AI and almost for free.
The main part - it’s personalized, because what is good for Bryan can be harmful for you!
Interested? Join our Longevity AI powered Guide
https://youtu.be/aj3bQa6gcOg
We do the same, but with AI and almost for free.
The main part - it’s personalized, because what is good for Bryan can be harmful for you!
Interested? Join our Longevity AI powered Guide
YouTube
This man ages backwards?
Bryan Johnson spends $2 million to become 18 again. And you won't believe how he is doing it!
Thank you Bryan Johnson for sharing your life with us!
And thank you to Lorena @sustentofila for telling this story!
Video credit: @BryanJohnson YouTube Channel…
Thank you Bryan Johnson for sharing your life with us!
And thank you to Lorena @sustentofila for telling this story!
Video credit: @BryanJohnson YouTube Channel…
ChatGPT Reviews in Longevity, Medicine and Science
ChatGPT is designed to understand and generate human-like text based on the patterns it has learned from a diverse range of internet sources. It can provide information, explanations, and engage in conversations on various subjects, including longevity, medicine, and science. However, it's important to note that while ChatGPT strives to provide accurate and up-to-date information, it may not always have access to the most recent research or breakthroughs in these fields since chatgpt training data only goes up until September 2021. Therefore, it's always a good idea to verify information from primary and authoritative sources.
Regarding longevity, ChatGPT can discuss general concepts and ideas related to extending human lifespan, such as the role of genetics, lifestyle factors, and advancements in medical technology. It can provide insights into the current understanding of aging processes, potential interventions, and ongoing research in the field. However, for specific medical advice or detailed discussions on cutting-edge longevity research, it's best to consult experts or refer to scientific literature.
In terms of medicine, ChatGPT can provide general information about various medical conditions, treatment options, and common practices. It can help explain medical terms, offer insights into symptoms, and discuss broad aspects of different diseases. However, it's essential to remember that ChatGPT is not a substitute for professional medical advice, diagnosis, or treatment. For personalized medical guidance or information, it's always advisable to consult qualified healthcare professionals.
Regarding science topics, ChatGPT can engage in discussions about a wide range of scientific disciplines, theories, and discoveries. It can provide explanations of scientific concepts, discuss historical scientific breakthroughs, and offer insights into various scientific fields. However, for specific scientific inquiries or highly specialized knowledge, it's recommended to consult subject-matter experts or refer to scientific literature.
It's worth noting that since ChatGPT knowledge cutoff is in September 2021, there may have been significant advancements or new discoveries in longevity, medicine, and science since then. So, it's always a good idea to supplement the information provided by ChatGPT with the most up-to-date and reliable sources available.
Overall, ChatGPT can be a useful tool to facilitate discussions, provide general information, and offer insights into various topics, including longevity, medicine, and science. However, it's important to exercise critical thinking, validate information from reliable sources, and consult domain experts for specific and authoritative knowledge in these fields
ChatGPT is designed to understand and generate human-like text based on the patterns it has learned from a diverse range of internet sources. It can provide information, explanations, and engage in conversations on various subjects, including longevity, medicine, and science. However, it's important to note that while ChatGPT strives to provide accurate and up-to-date information, it may not always have access to the most recent research or breakthroughs in these fields since chatgpt training data only goes up until September 2021. Therefore, it's always a good idea to verify information from primary and authoritative sources.
Regarding longevity, ChatGPT can discuss general concepts and ideas related to extending human lifespan, such as the role of genetics, lifestyle factors, and advancements in medical technology. It can provide insights into the current understanding of aging processes, potential interventions, and ongoing research in the field. However, for specific medical advice or detailed discussions on cutting-edge longevity research, it's best to consult experts or refer to scientific literature.
In terms of medicine, ChatGPT can provide general information about various medical conditions, treatment options, and common practices. It can help explain medical terms, offer insights into symptoms, and discuss broad aspects of different diseases. However, it's essential to remember that ChatGPT is not a substitute for professional medical advice, diagnosis, or treatment. For personalized medical guidance or information, it's always advisable to consult qualified healthcare professionals.
Regarding science topics, ChatGPT can engage in discussions about a wide range of scientific disciplines, theories, and discoveries. It can provide explanations of scientific concepts, discuss historical scientific breakthroughs, and offer insights into various scientific fields. However, for specific scientific inquiries or highly specialized knowledge, it's recommended to consult subject-matter experts or refer to scientific literature.
It's worth noting that since ChatGPT knowledge cutoff is in September 2021, there may have been significant advancements or new discoveries in longevity, medicine, and science since then. So, it's always a good idea to supplement the information provided by ChatGPT with the most up-to-date and reliable sources available.
Overall, ChatGPT can be a useful tool to facilitate discussions, provide general information, and offer insights into various topics, including longevity, medicine, and science. However, it's important to exercise critical thinking, validate information from reliable sources, and consult domain experts for specific and authoritative knowledge in these fields
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Mike Lustgarten, PhD - Telomere Length Test #6: Correlations With Diet https://youtu.be/gWeht1QdpLc
YouTube
Telomere Length Test #6: Correlations With Diet
Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD
Discount Links:
Telomere Length, Epigenetic Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ62UkAVXBWtRVKJUM0&irgwc=1
Use Code: CONQUERAGING
NAD+ Quantification: http…
Discount Links:
Telomere Length, Epigenetic Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ62UkAVXBWtRVKJUM0&irgwc=1
Use Code: CONQUERAGING
NAD+ Quantification: http…
Very interesting, new in vivo aspects of the mitochondrial metabolisms role for cell fate and differentiation, transdifferentiation potential, cancer stem cells https://phys.org/news/2023-06-uncovers-clues-cell-plasticity.html
phys.org
Study uncovers new clues about the process of cell plasticity
Researchers have long thought that once a cell starts down its path of differentiation, growing into a skin cell or a liver cell or a neuron, that path could not be changed.
The long-awaited video of Gero CEO Peter Fedichev's speech at Zuzalu can now be viewed at: https://zuzalu.streameth.org/session/869 . For more detailed information about Gero's latest findings on the fundamentals of aging, check out the article "Humans Can Stop—But Not Fully Reverse—Aging" in Popular Mechanics: https://www.popularmechanics.com/science/health/a43510158/humans-can-stop-aging-but-not-reverse-it-study/
The next round of interesting public talks between Peter Fedichev and Aubrey De Grey on general prospects and Gero's plans on stopping aging, as well as about the limits of age reversal , is expected to take place in Dublin https://longevitysummitdublin.com/.
The world is changing, so stay tuned for updates. You can follow Gero.ai on
https://www.facebook.com/geroscience
www.linkedin.com/company/4994380
https://twitter.com/GeroMaxim
https://www.crunchbase.com/organization/gero/signals_and_news
The next round of interesting public talks between Peter Fedichev and Aubrey De Grey on general prospects and Gero's plans on stopping aging, as well as about the limits of age reversal , is expected to take place in Dublin https://longevitysummitdublin.com/.
The world is changing, so stay tuned for updates. You can follow Gero.ai on
https://www.facebook.com/geroscience
www.linkedin.com/company/4994380
https://twitter.com/GeroMaxim
https://www.crunchbase.com/organization/gero/signals_and_news
Zuzalu city
Aging clocks, entropy, and the limits of age-reversal · Zuzalu city
Zuzalu is a first-of-its-kind pop-up city community in Montenegro.