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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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human lifespan
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human lifespan and longevity
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đ Study Purpose
The research investigates how m đ Study Purpose
The research investigates how much genetics influences human lifespan, and whether the importance of genes increases, decreases, or stays constant with age.
Twin studies are used because comparing identical (MZ) and fraternal (DZ) twins can separate genetic from environmental effects.
𧏠Key Findings (Very Clear Summary)
1ď¸âŁ Genetics explains about 20â30% of lifespan differences
Previous studies showed this, and the current paper confirms it.
2ď¸âŁ Genetic influence is minimal before age 60
Before age 60, MZ and DZ twins show almost no difference in how long they live.
Meaning: environment and random events dominate early-life and mid-life survival.
3ď¸âŁ After age 60, genetic influence becomes strong
After about 60 years:
Identical twinsâ lifespans rise and fall together much more strongly than fraternal twinsâ.
This shows that genes increasingly shape survival at older ages.
Example:
For every extra year an MZ twin lives past 60, the other lives 0.39 extra years.
For DZ twins, this number is only 0.21 years.
4ď¸âŁ Chance of reaching very old age is far more similar in MZ twins
At age 92:
MZ male twins are 4.8Ă more likely to both reach age 92 than expected by chance.
DZ male twins are only 1.8Ă more likely.
Female patterns are similar but shifted ~5â10 years later (women live longer).
5ď¸âŁ Genetic effects remain strong even among people who already survived to age 75
In a special group where both twins already lived to 75, MZ twins remain significantly more similar than DZ twins up to age 92.
This confirms:
đ Genetic influence on longevity does NOT disappear at extreme ages.
𧪠Data Sources
The study uses 20,502 twins from:
Denmark
Sweden
Finland
Born 1870â1910, followed for 90+ years.
This is one of the largest and most complete longevity twin datasets ever collected.
đ Methods Summary
Two major analysis types:
1. Conditional Lifespan
âHow long does one twin live, depending on how long the co-twin lived?â
This detects lifespan similarity.
2. Survival to a Given Age
Twin pairs were checked for:
Relative recurrence risk (RRR) â How much more likely a twin reaches age X if the co-twin did?
Tetrachoric correlation â A statistical measure of shared liability for survival.
Both consistently showed stronger resemblance in MZ twins at older ages.
đ§ Interpretation
What the results mean
Before age 60: Mostly accidents, lifestyle, environment â genetic influence weak.
After age 60: Survival depends more on biologyâaging pathways, resistance to diseases, cell repair, etc.
Supports two big ideas:
Genetic influence increases with age for surviving to old ages.
Late-life survival is influenced by:
âLongevity enabling genesâ
Genes reducing disease risks
Genes protecting overall health at old ages
𧊠Why It Matters
This study provides scientific justification for ongoing searches for:
Longevity genes
Aging pathway genes
Genetic biomarkers of healthy aging
It also shows that:
đ Genetics matters most not for reaching 60⌠but for reaching 80, 90, or 100+.
đ Perfect One-Sentence Summary
Genetic influence on human lifespan is small before age 60 but becomes increasingly strong afterward, making genes a major factor in reaching very old ages....
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meuvcaig-6493
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xevyo
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humans in 21st century
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humans in the twenty-first century
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Implausibility of Radical Life Extension in Humans Implausibility of Radical Life Extension in Humans in the Twenty-First Century
Human in 21st century
This study, published in Nature Aging (2024), analyzes real demographic data from the worldâs longest-lived populations to determine whether radical human life extension is occurringâor likely to occurâin this century. The authors conclude that radical life extension is not happening and is biologically implausible unless we discover ways to slow biological aging itself, not just treat diseases.
đ§ 1. Central Argument
Over the 20th century, life expectancy grew rapidly due to public health and medical advances. But since 1990, improvements in life expectancy have slowed dramatically across all longest-lived nations.
Human in 21st century
The core message:
Unless aging can be biologically slowed, humans are already near the upper limits of natural life expectancy.
Human in 21st century
đ 2. Has Radical Life Extension Happened?
The authors define radical life extension as:
đ A 0.3-year increase in life expectancy per year (3 years per decade) â similar to gains during the 20th-century longevity revolution.
Using mortality data from 1990â2019 (Australia, France, Italy, Japan, South Korea, Spain, Sweden, Switzerland, Hong Kong, USA):
đ´ Findings:
Only Hong Kong and South Korea briefly approached this rate (mostly in the 1990s).
Every country shows slowed growth in life expectancy since 2000.
Human in 21st century
The U.S. even experienced declines in life expectancy in recent decades due to midlife mortality.
Human in 21st century
đŻ 3. Will Most People Today Reach 100?
The data say no.
Actual probabilities of reaching age 100:
Females: ~5%
Males: ~1.8%
Highest observed: Hong Kong (12.8% females, 4.4% males)
Human in 21st century
Nowhere near the 50% survival to 100 predicted by âradical life extensionâ futurists.
đ 4. How Hard Is It to Increase Life Expectancy Today?
To add just one year to life expectancy, countries now must reduce mortality at every age by far more than in the past.
Example: For Japanese females (2019):
To go from 88 â 89 years requires
đ 20.3% reduction in death rates at ALL ages.
Human in 21st century
These reductions are increasingly unrealistic using current medical approaches.
𧏠5. Biological & Demographic Constraints
Three demographic signals show humans are approaching biological limits:
A. Life table entropy (H*) is stabilizing
Shows mortality improvements are becoming harder.
Human in 21st century
B. Lifespan inequality (ÎŚ*) is decreasing
Deaths are increasingly compressed into a narrow age window â meaning humans are already dying close to the biological limit.
Human in 21st century
C. Maximum lifespan has stagnated
No increase beyond Jeanne Calmentâs record of 122.45 years.
Human in 21st century
Together, these metrics prove that life expectancy gains are slowing because humans are nearing biological constraintsânot because progress in medicine has stopped.
đŤ 6. What Would Radical Life Extension Require?
The authors create a hypothetical future where life expectancy reaches 110 years.
To achieve this:
70% of females must survive to 100
24% must survive beyond 122.5 (breaking the maximum human lifespan)
6â7% must live to 150
Human in 21st century
This would require:
88% reduction in death rates at every age up to 150
Human in 21st century
This is impossible using only disease treatment. It would require curing most causes of death.
đ 7. Composite âBest-Caseâ Mortality Worldwide
The authors compile the lowest death rates ever observed in any country (2019):
Best-case female life expectancy: 88.7 years
Best-case male life expectancy: 83.2 years
Human in 21st century
Even with zero deaths from birth to age 50, life expectancy increases by only one additional year.
Human in 21st century
This shows why further increases are extremely difficult.
đ§ 8. Final Conclusions
Radical life extension is not happening in todayâs long-lived nations.
Biological and demographic forces limit life expectancy to about 85â90 years for populations.
Survival to 100 will remain rare (around 5â15% for females; 1â5% for males).
Treating diseases alone cannot extend lifespan dramatically.
Only slowing biological aging (geroscience) could meaningfully shift these limits.
Human in 21st century
đ Perfect One-Sentence Summary
Humanity is already near the biological limits of life expectancy, and radical life extension in the 21st century is implausible unless science discovers ways to slow the fundamental processes of aging....
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xksnrvow-7963
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xevyo
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identification of
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identification of a geographic
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This study presents a rigorous demographic investi This study presents a rigorous demographic investigation that identifies and validates a unique region of exceptional human longevity on the island of Sardiniaâknown today as one of the worldâs first confirmed Blue Zones. Using verified birth, marriage, and death records from 377 municipalities, the researchers introduce the Extreme Longevity Index (ELI) to measure the probability that individuals born between 1880 and 1900 reached age 100.
The analysis reveals a distinct cluster in the mountainous central-eastern region of Sardinia where the likelihood of becoming a centenarian is dramatically higher than the island average. This âBlue Zoneâ displays not only elevated longevity but also an extraordinary male-to-female centenarian ratio, including areas where men outnumber female centenariansâan unprecedented finding in global longevity research.
Through Gaussian spatial smoothing and chi-square testing, the authors demonstrate that this longevity pattern is statistically significant, geographically coherent, and unlikely to be due to random variation or data error. The study discusses potential explanations: long-term geographic isolation, low immigration, high rates of endogamy, a culturally preserved lifestyle, traditional diet, and genetic homogeneity that may confer protection against age-related diseases.
The paper concludes that the Sardinian Blue Zone is a scientifically validated longevity hotspot and calls for further genetic, cultural, and environmental studies to uncover the mechanisms that support such exceptional survival patterns.
...
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c583a8f4-b052-41d6-ab2c-24afe829f9ae
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qdzwhpef-1289
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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longevity lifespain
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longevity across the human life span
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âSocial relationships and physiological determinan âSocial relationships and physiological determinants of longevity across the human life spanâ is a landmark study that explains how social relationships directly shape the biology of aging, beginning in adolescence and persisting into old age. Using an unprecedented integration of four major U.S. longitudinal datasets, the authors show that social connections literally âget under the skin,â altering inflammation, cardiovascular function, metabolic health, and ultimately lifespan.
The study examines two key dimensions of social relationships:
Social integration â the quantity of social ties and frequency of interaction
Social support and strain â the quality, positivity, or negativity of those relationships
Across adolescence, young adulthood, midlife, and late adulthood, the researchers link these measures to objective biomarkers: CRP inflammation, blood pressure, waist circumference, and BMI.
Core Findings
More social connections = better physiological health, in a clear doseâresponse pattern.
Social isolation is as biologically harmful as major clinical risks.
In adolescence, isolation increased inflammation as much as physical inactivity.
In old age, its impact on hypertension exceeded that of diabetes.
Effects emerge early and accumulate: adolescent social integration predicts cardiovascular and metabolic health years later.
Midlife is different: quantity of relationships matters less, but quality (support or strain) becomes especially important.
Negative relationships (strain) are stronger predictors of poor health than lack of support.
Late-life social connections protect against hypertension and obesity, even after adjusting for demographics, behavior, and socioeconomic factors.
Significance
The study provides some of the strongest evidence to date that social relationships causally influence longevity through biological pathways, not just through behavior or psychology. It shows that:
Social connectedness is a lifelong biological asset.
Social adversity is a chronic physiological stressor that accelerates aging.
Effective health and longevity strategies must include social environments, not just medical or lifestyle interventions.
This work fundamentally reframes longevity research by demonstrating that aging is shaped not only by genes, lifestyle, or medical careâbut also by the structure and quality of our social lives....
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vzblqkgd-9030
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xevyo
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longevity by preventing
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longevity by preventing the age
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This scientific paper, published in PLOS Biology ( This scientific paper, published in PLOS Biology (2025), investigates how removing the protein Maf1âa natural repressor of RNA Polymerase IIIâin neurons can significantly extend lifespan and improve age-related health in Drosophila melanogaster (fruit flies). The study focuses on how aging reduces the ability of neurons to perform protein synthesis, and how reversing this decline affects longevity.
Core Scientific Insight
Maf1 normally suppresses the production of small, essential RNA molecules (like 5S rRNA and tRNAs) needed for building ribosomes and synthesizing proteins. Aging decreases protein synthesis in many tissues including the brain. This study shows that removing Maf1 specifically from adult neurons increases Pol III activity, boosts production of 5S rRNA, maintains protein synthesis, and ultimately promotes healthier aging and longer life.
Major Findings
Knocking down Maf1 in adult neurons extends lifespan, in both female and male flies, with larger effects in females.
Longevity effects are cell-type specific: extending lifespan works via neurons, not gut or fat tissues.
Neuronal Maf1 removal:
Delays age-related decline in motor function
Improves sleep quality in aged flies
Protects the gut barrier from age-related failure
Aging naturally causes a sharp decline in 5S rRNA levels in the brain. Maf1 knockdown prevents this decline.
Maf1 depletion maintains protein synthesis rates in old age, which normally fall significantly.
Longevity requires Pol III initiation on 5S rRNAâgenetically blocking this eliminates the life-extending effect.
The intervention also reduces toxicity in a fruit-fly model of C9orf72 neurodegenerative disease (linked to ALS and FTD), highlighting potential therapeutic importance.
Biological Mechanism
Removing Maf1 â increased Pol III activity â restored 5S rRNA levels â increased ribosome functioning â maintained protein synthesis â improved neuronal and systemic health â extended lifespan.
Broader Implications
The study challenges the long-standing assumption that reducing translation always extends lifespan. Instead, it reveals a cell-typeâspecific benefit: neurons, unlike other tissues, require sustained translation for healthy aging. The findings suggest similar mechanisms may exist in mammals, potentially offering insights into combatting neurodegeneration and age-related cognitive decline....
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vgsshyvs-3844
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xevyo
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longevity in mammals
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longevity in mammals
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This PDF is a high-level evolutionary biology rese This PDF is a high-level evolutionary biology research article published in PNAS that investigates why some mammals live longer than others. It tests a powerful hypothesis:
Mammals that live in trees (arboreal species) evolve longer lifespans because tree-living reduces external sources of death such as predators, disease, and environmental hazards.
Using a massive dataset of 776 mammalian species, the study compares lifespan, body size, and habitat across nearly all mammalian clades. It provides one of the strongest empirical tests of evolutionary ageing theory in mammals.
The core message:
Arboreal mammals live significantly longer than terrestrial mammals, even after accounting for body size and evolutionary history â supporting the evolutionary theory of ageing and clarifying why primates (including humans) evolved long lifespans.
đł 1. Why Arboreality Should Increase Longevity
Evolutionary ageing theory predicts:
High extrinsic mortality (predators, disease, accidents) â earlier ageing, shorter lifespan
Low extrinsic mortality â slower ageing, longer lifespan
Tree living offers protection:
Harder for predators to attack
Less exposure to ground hazards
Improved escape options
Therefore, species that spend more time in trees should evolve greater lifespan and delayed senescence.
Longevity in mammals
đ 2. Dataset and Methodology
The paper analyzes:
776 species of non-flying, non-aquatic mammals
Lifespan records (mostly from captive data for accurate maxima)
Species classified into:
Arboreal
Semiarboreal
Terrestrial
Body mass as a key covariate
Phylogenetically independent contrasts (PIC) to remove evolutionary bias
This allows a robust test of whether habitat causes differences in longevity.
Longevity in mammals
đ 3. Main Findings
â A. Arboreal mammals live longer
Across mammals, tree-living species have significantly longer maximum lifespans than terrestrial ones when body size is held constant.
Longevity in mammals
â B. The pattern holds in most mammalian groups
In 8 out of 10 subclades, arboreal species live longer than terrestrial relatives.
â C. Exceptions reveal evolutionary history
Two groups do not show this pattern:
Primates & Their Close Relatives (Euarchonta)
Arboreal and terrestrial species do not differ significantly
Likely because primates evolved from highly arboreal ancestors
Their long lifespan may have been established early and retained
Even terrestrial primates inherit long-living traits
Longevity in mammals
Marsupials (Metatheria)
No longevity advantage for arboreal vs. terrestrial species
Marsupials in general are not long-lived, regardless of habitat
Longevity in mammals
â D. Squirrels provide a clear example
Within Sciuroidea:
Arboreal squirrels live longer than terrestrial squirrels
Semiarboreal species fall in between
Longevity in mammals
đ 4. Why Primates Are a Special Case
The article provides an important evolutionary insight:
Primates did not gain longevity from becoming arboreal â they were already arboreal.
Arboreality is the ancestral primate condition
Long lifespan likely evolved early as primates adapted to tree life
Later terrestrial primates (baboons, humans) retained this long-lived biology
Additional survival strategies (large body size, social structures, intelligence) further reduce predation
Longevity in mammals
This helps explain why humansâthe most terrestrial primateâstill have extremely long lifespans.
𧏠5. Evolutionary Significance
The study strongly supports evolutionary ageing theory:
Low extrinsic mortality â slower ageing
Arboreality functions like a protective âlife-extending shieldâ
Similar patterns seen in flying mammals (bats) and gliding mammals
Reduced risk environments create selection pressure for longer lives
Longevity in mammals
đž 6. Additional Insights
âď¸ Body size explains ~60% of lifespan variation
Larger mammals generally live longer, but habitat explains additional differences.
âď¸ Arboreal habitats evolve multiple times
Many mammal groups that shifted from ground to trees repeatedly evolved greater longevity â independently.
âď¸ Sociality reduces predation too
Large social groups (e.g., in primates and some marsupials) reduce predator risk, altering ageing patterns.
Longevity in mammals
â Overall Summary
This PDF provides a groundbreaking comparative analysis showing that arboreal mammals live longer than terrestrial mammals, validating key predictions of evolutionary ageing theory. It demonstrates that reduced exposure to predators and environmental hazards in tree habitats leads to delayed ageing and increased lifespan. While most mammals follow this pattern, primates and marsupials are exceptions due to their unique evolutionary histories â particularly primates, who long ago evolved the long-living biology that humans still carry today.
This study is one of the most compelling demonstrations of how ecology, behavior, and evolutionary history shape lifespan across mammals....
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wvptnahr-9268
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longevity of C. elegans m
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longevity of C. elegans mutants
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This study delivers a deep, mechanistic explanatio This study delivers a deep, mechanistic explanation of how changes in lipid biosynthesisâspecifically in fatty-acid chain length and saturationâcontribute directly to the extraordinary longevity of certain C. elegans mutants, especially those with disrupted insulin/IGF-1 signaling (IIS). By comparing ten nearly genetically identical worm strains that span a tenfold range of lifespans, the authors identify precise lipid signatures that track strongly with lifespan and experimentally confirm that altering these lipid pathways causally extends or reduces lifespan.
Its central insight:
Long-lived worms reprogram lipid metabolism to make their cell membranes more resistant to oxidative damage, particularly by reducing peroxidation-prone polyunsaturated fatty acids (PUFAs) and shifting toward shorter and more saturated lipid chains.
This metabolic remodeling lowers the substrate available for destructive free-radical chain reactions, boosting both stress resistance and lifespan.
𧏠Core Findings, Explained Perfectly
1. Strong biochemical patterns link lipid structure to lifespan
Across all strains, two lipid features were the strongest predictors of longevity:
A. Shorter fatty-acid chain length
Long-lived worms had:
more short-chain fats (C14:0, C16:0)
fewer long-chain fats (C18:0, C20:0, C22:0)
Average chain length decreased almost perfectly in proportion to lifespan.
B. Fewer polyunsaturated fatty acids (PUFAs)
Long-lived mutants had:
sharply reduced PUFAs (EPA, arachidonic acid, etc.)
dramatically lower peroxidation index (PI)
fewer double bonds (lower DBI)
These changes make membranes much less susceptible to lipid peroxidation damage.
2. Changes in enzyme activity explain the lipid shifts
By measuring mRNA levels and inferred enzymatic activity, the study shows:
Downregulated in long-lived mutants
Elongases (elo-1, elo-2, elo-5) â shorter chains
Î5 desaturase (fat-4) â fewer PUFAs
Upregulated
Î9 desaturases (fat-6, fat-7) â more monounsaturated, oxidation-resistant MUFAs
This combination produces membranes that are:
just fluid enough (thanks to MUFAs)
much harder to oxidize (thanks to less PUFA content)
This is a perfect, balanced redesign of the membrane.
3. RNAi experiments prove these lipid changes CAUSE longevity
Knocking down specific genes in normal worms produced dramatic effects:
Increasing lifespan
fat-4 (Î5 desaturase) RNAi â +25% lifespan
elo-1 or elo-2 (elongases) RNAi â ~10â15% lifespan increase
Combined elo-1 + elo-2 knockdown â even larger increase
Reducing lifespan
Knockdown of Î9 desaturases (fat-6, fat-7) slightly shortened lifespan
Stress resistance matched the lifespan effects
The same interventions boosted survival under hydrogen peroxide oxidative stress, confirming that resistance to lipid peroxidation is a key mechanism of longevity.
4. Dietary experiments confirm the same mechanism
When worms were fed extra PUFAs like EPA or DHA:
lifespan dropped by 16â24%
Even though these fatty acids are often considered âhealthyâ in humans, in worms they create more oxidative vulnerability, validating the model.
5. Insulin/IGF-1 longevity mutants remodel lipids as part of their longevity program
The longest-lived mutantsâespecially age-1(mg44), which can live nearly 10Ă longerâshow the greatest lipid remodeling:
lowest elongase expression
lowest PUFA levels
highest MUFA-producing Î9 desaturases
This suggests that IIS mutants extend lifespan partly through targeted remodeling of membrane lipid composition, not just through metabolic slowdown or stress-response pathways.
đĄ What This Means
The core conclusion
Longevity in C. elegans is intimately connected to reducing lipid peroxidation, a major source of cellular damage.
Worms extend their lifespan by:
shortening lipid chains
reducing PUFA content
elevating MUFAs
suppressing enzymes that create vulnerable lipid species
enhancing enzymes that create stable ones
These changes:
harden membranes against oxidation
reduce chain-reaction damage
increase survival under stress
extend lifespan significantly
**This is one of the clearest demonstrations that lipid composition is not just correlated with longevityâ
it helps cause longevity.**...
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hiynnkoy-3916
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xevyo
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mtorc1 is also involve in
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mtorc1 is also involve in longevity between specie
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This PDF is a scientific editorial from the journa This PDF is a scientific editorial from the journal Aging (2021) that explains how mTORC1, a central nutrient- and energy-sensing cellular pathway, plays a critical role not only in lifespan extension within a single species but also in determining natural longevity differences between mammalian species.
The authors, Gustavo Barja and Reinald Pamplona, summarize recent comparative research showing that long-lived species naturally maintain lower mTORC1 activity, suggesting that downregulated mTORC1 signaling is an evolutionary adaptation that contributes to slower aging and extended longevity.
đś 1. Background: The Aging Program & Effector Systems
The paper begins by reviewing the nuclear aging program (AP) and the network of aging effectors controlled by it.
These include:
mitochondrial ROS production
mitochondrial DNA repair
lipid composition of membranes
telomere shortening rates
metabolomic/lipidomic profiles
mTORC1 is also involved in longâŚ
Long-lived species show:
low mitochondrial ROS at complex I
high mitochondrial DNA repair
lower unsaturated fatty acids in membranes
slower telomere shortening
mTORC1 is also involved in longâŚ
These differences shape species-specific aging rates.
đś 2. What is mTORC1 and Why It Matters for Aging?
mTORC1 is a highly conserved cellular signaling hub that integrates information about:
nutrients
energy (ATP, glucose)
amino acids (especially arginine, leucine, methionine)
hormones
oxygen levels
mTORC1 is also involved in longâŚ
mTORC1 regulates:
protein + lipid synthesis
mitochondrial function
autophagy
cell growth and proliferation
stress responses
Within species, lowering mTORC1 activity increases lifespan in yeast, worms, flies, and mammals, while increased mTORC1 accelerates aging.
đś 3. The New Study: First Cross-Species Analysis of mTORC1 and Longevity
The editorial highlights a new comparative study across eight mammalian species with lifespans ranging from 3.5 years (mouse) to 46 years (horse).
Using droplet digital PCR (ddPCR), Western blotting, and targeted metabolomics, the study measured:
mTORC1 gene expression
mTORC1 protein levels
concentrations of activators and inhibitors
mTORC1 is also involved in longâŚ
đś 4. Key Findings: Long-Lived Species Naturally Suppress mTORC1
The study found that longer-living mammals consistently exhibit a molecular signature of low mTORC1 activity, including:
A) Activators â (negatively correlated with longevity)
Long-lived species have low levels of:
mTOR
Raptor
Arginine
Methionine
SAM (S-adenosylmethionine)
Homocysteine
mTORC1 is also involved in longâŚ
B) Inhibitors â (positively correlated with longevity)
Long-lived species have higher levels of:
phosphorylated mTOR (mTORSer2448)
PRAS40
mTORC1 is also involved in longâŚ
These patterns were independent of phylogeny, meaning they reflect functional longevity mechanisms, not ancestry.
đś 5. Interpretation: mTORC1 Is Part of an Evolutionary Longevity Strategy
The authors argue that:
Long-lived species have evolved permanent, natural repression of mTORC1 signaling.
This protects cells from accelerated aging, degenerative diseases, and metabolic stress.
mTORC1 works in coordination with other aging effectors as part of the Cell Aging Regulating System (CARS).
mTORC1 is also involved in longâŚ
This places mTORC1 as a cross-species determinant of longevity, not just a within-species modulator.
đś 6. Overall Conclusion
The PDF concludes that maintaining low mTORC1 downstream activity during adult life is a conserved biological strategy that increases longevity both within and between mammalian species. This is the first study to show that natural variation in mTORC1 levels across species correlates directly with evolutionary differences in lifespan.
â Perfect One-Sentence Summary
This editorial explains that long-lived mammalian species naturally suppress mTORC1 activityâthrough lower levels of its activators and higher levels of its inhibitorsârevealing mTORC1 as a fundamental, evolutionarily conserved determinant of species longevity....
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gsazhjdx-7806
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xevyo
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signs of life guidance
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signs of life guidance
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âSigns of Life Guidance â Visual Summary (v1.2)â i âSigns of Life Guidance â Visual Summary (v1.2)â is a clear, compassionate, UK-wide clinical guideline that explains how to determine and document signs of life following spontaneous birth before 24+0 weeks, in situations whereâafter careful discussion with the parentsâactive survival-focused neonatal care is not appropriate. The guidance ensures consistent, respectful, and trauma-minimizing care for both babies and parents during extremely preterm births.
Purpose of the Guidance
To help clinicians:
Recognize genuine signs of life
Communicate sensitively with parents
Provide appropriate comfort and palliative care
Ensure correct legal documentation of birth and death
Deliver consistent bereavement support across the UK
Determining Signs of Life
A baby is classified as liveborn if any of the following visible, persistent signs are present:
clearly visible heartbeat
visible cord pulsation
breathing, crying, or sustained gasps
definite limb movement
The guidance emphasizes:
Fleeting reflexes (brief gasps, twitches, or chest wall pulsations in the first minute) do not count as signs of life.
Parentsâ own observations should be respectfully included.
A stethoscope is not required.
After Live Birth
A doctor (usually the obstetrician) should confirm and document signs of life to avoid legal complications with the death certificate.
A doctor may rely on a midwifeâs documented observations.
The baby receives perinatal palliative comfort care, and the familyâs emotional and physical needs are actively supported.
Communication With Parents
Sensitive communication is emphasized to reduce trauma:
Parents are prepared that babies born before 24 weeks often do not survive.
Parents are informed that reflex movements do not necessarily indicate life.
Language preferences must be respectedâsome parents prefer âloss of baby,â others prefer âend of pregnancyâ or âmiscarriage.â
Bereavement Care (All Births)
All families should receive:
A parent-led bereavement plan
Privacy, choices, and time with their baby
Memory-making opportunities
Information on burial/cremation/sensitive disposal
Referral to support services and community care
Guidelines reference the National Bereavement Care Pathway for consistent care across the UK.
Documentation Requirements
Depends on region and whether signs of life were witnessed:
Before 24+0 weeks: No legal requirement for birth registration; offer a sensitive âcertificate of lossâ or âcertificate of birth.â
If liveborn and later dies: A neonatal death certificate must be issued by a doctor who witnessed signs of life.
If no doctor witnessed it, the case must be referred to the coroner in England/Wales/NI.
Scope of the Guidance
Included:
Spontaneous in-hospital births <22+0 weeks
Spontaneous births at 22+0 to 23+6 weeks when survival-focused care is not appropriate
Pre-hospital births <22+0 weeks (same principles)
Excluded:
>Medical terminations
>Uncertain gestational age
>Births at 22â23+6 weeks where active neonatal care is planned or considered...
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nnequewi-7486
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the molecular signatures
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the molecular signatures of longevity
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âThe Molecular Signatures of Longevityâ is a compr âThe Molecular Signatures of Longevityâ is a comprehensive scientific review that explores the shared biological patternsâor âsignaturesââthat distinguish long-lived organisms from normal ones, across species ranging from yeast and worms to mice and humans. The paper synthesizes genomic, transcriptomic, proteomic, metabolic, and epigenetic evidence to uncover the molecular hallmarks that consistently support longer lifespan and extended healthspan.
Core Idea
Long-lived species, long-lived mutants, and exceptionally long-lived humans (like centenarians) share a set of convergent molecular features. These signatures reflect a body that ages more slowly because it prioritizes maintenance, protection, and metabolic efficiency over growth and reproduction.
Major Molecular Signatures Identified
1. Downregulated growth-related pathways
Across almost all models of longevity, genes that drive growth and proliferationâsuch as insulin/IGF-1 signaling, mTOR, and growth hormone pathwaysâare consistently reduced.
This metabolic shift favors stress resistance and preservation, not rapid cell division.
2. Enhanced stress-response and repair systems
Long-lived organisms upregulate genes and pathways that improve:
>DNA repair
>Protein folding and quality control
>Antioxidant defenses
>Cellular detoxification
These changes help prevent molecular damage and maintain cellular integrity over decades.
Determinants of Longevity
3. Improved mitochondrial function and energy efficiency
Longevity is associated with:
More efficient mitochondria
Altered electron transport patterns
Reduced reactive oxygen species (ROS) production
Rather than producing maximum energy, long-lived organisms produce steady, clean energy that minimizes internal damage.
Determinants of Longevity
4. Reduced chronic inflammation
A consistent signature of long-lived humansâincluding centenariansâis low baseline inflammation (inflammaging avoidance).
They show lower activation of immune-inflammatory pathways and better regulation of cytokine responses.
5. Epigenetic stability
Long-lived individuals maintain:
Younger DNA methylation patterns
Stable chromatin structure
Preserved transcriptional regulation
These allow their cells to âbehave youngerâ despite chronological age.
Insights from Centenarians
Centenarians display many of the same molecular signatures found in long-lived animal models:
Exceptional lipid metabolism, especially in pathways involving APOE
Robust immune regulation, avoiding chronic inflammation
Gene expression profiles resembling people decades younger
Protective metabolic and repair pathways that remain active throughout life
They often appear biologically resilient, maintaining molecular systems that typically erode with aging.
Determinants of Longevity
Evolutionary Perspective
The article explains that these longevity signatures arise because evolution favors maintenance and efficiency in certain species where survival under stress is essential.
Thus, the same metabolic and stress-response systems that help organisms survive harsh conditions also extend lifespan.
Implications for Human Health and Interventions
The paper highlights that several known anti-aging interventionsâsuch as calorie restriction, rapamycin, fasting, metformin, and certain genetic variantsâwork largely because they activate the same molecular signatures found in naturally long-lived organisms.
These shared signatures point toward potential therapeutic targets, including:
IGF-1 / mTOR inhibition
Enhanced DNA repair
Mitochondrial optimization
Anti-inflammatory modulation
Epigenetic rejuvenation
Conclusion
âThe Molecular Signatures of Longevityâ shows that longevity is not randomâit has a repeatable, identifiable molecular blueprint.
Across species and in exceptionally long-lived humans, the same biological themes appear:
Less growth, more protection. Less inflammation, more repair. Cleaner energy, stronger stress resistance.
These convergent signatures reveal the fundamental biology of long life and offer a roadmap for extending human healthspan through targeted interventions....
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8b6251b9-8b61-43c1-a7b5-551242fd8b71
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prrpbudm-6958
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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The Biomarkers in Extreme
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âThe Biomarkers in Extreme Longevity
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âThe Biomarkers in Extreme Longevityâ is a scienti âThe Biomarkers in Extreme Longevityâ is a scientific investigation into the biological signaturesâgenetic, metabolic, cellular, and physiologicalâthat distinguish centenarians and supercentenarians from the general population. The paper systematically reviews which biomarkers reliably predict exceptional lifespan and which biological systems remain unusually preserved in individuals who live beyond 100 years.
The Biomarkers in Extreme LongeâŚ
The study positions extreme longevity not as a random occurrence, but as a measurable phenotype marked by distinctive patterns of inflammation, immune function, metabolism, cellular aging, and genetic resilience.
Core Themes and Findings
1. Centenarians Are Unusually Healthy for Their Age
The paper emphasizes that extreme longevity is strongly associated with compression of morbidityâmost centenarians delay major diseases until very late in life.
Several health indicators (cognitive function, cardiometabolic stability, physical performance) remain better preserved than expected for advanced age.
The Biomarkers in Extreme LongeâŚ
2. Inflammation Is the Most Predictive Biomarker
A central conclusion of the study:
Chronic low-grade inflammation (âinflammagingâ) is the single most powerful predictor of death and chronic disease in the oldest-old.
The Biomarkers in Extreme LongeâŚ
Centenarians show:
Lower inflammatory cytokines
Better-controlled immune activation
Strong anti-inflammatory signaling pathways
This moderated inflammatory state distinguishes them from age-matched controls.
3. Immune System Robustness Is a Key Longevity Signature
Centenarians maintain:
Better adaptive immune function
Higher levels of protective immune cells
Enhanced response to pathogens
This combination allows them to survive infections and stressors that typically cause mortality in late old age.
The Biomarkers in Extreme LongeâŚ
4. Genetic Biomarkers Strongly Influence Extreme Longevity
The paper highlights several genetic factors linked to surviving past 100:
Protective variants in FOXO3A
Favorable lipid metabolism genes
Variants regulating DNA repair and cellular stress response
The genetic component is substantialâcentenarians often have offspring with lower mortality risk, demonstrating hereditary resilience.
5. Metabolic Biomarkers Are Uniquely Optimized
Centenarians typically show:
Better lipid profiles
Lower insulin resistance
Superior glucose control
These metabolic patterns correspond with reduced cardiovascular and diabetic risk well into old age.
6. Telomere Length Is Not the Main Longevity Marker
Contrary to popular belief, the paper notes:
Telomere length is not consistently longer in centenarians.
Instead, centenarians appear to possess mechanisms that protect cells despite telomere shortening, suggesting cellular resilience is more important than raw telomere length.
7. Epigenetic âYouthfulnessâ Predicts Exceptional Longevity
The study reviews evidence that extreme longevity is associated with:
Slower epigenetic clock aging
More stable DNA methylation patterns
Delayed age-related drift in key gene pathways
These epigenetic signatures may serve as early-life predictors of who reaches 100+.
The Biomarkers in Extreme LongeâŚ
8. Cardiovascular Biomarkers Are Particularly Protective
Centenarians often show:
Better endothelial function
Lower arterial stiffness
Preserved heart rate variability
These protective cardiovascular markers may explain their low rates of heart disease until very late in life.
Overall Interpretation
Extreme longevity is characterized by a cluster of interrelated biomarkers, including:
low chronic inflammation
strong immune resilience
optimized lipid and glucose metabolism
protective gene variants
youthful epigenetic profiles
preserved cardiovascular health
delayed functional decline
The paper concludes that these biomarkers create a biological phenotype that allows centenarians to avoid or postpone major diseases decades longer than average.
Conclusion
âThe Biomarkers in Extreme Longevityâ presents a unified scientific framework for understanding why some individuals live to 100â110+ years.
The study shows that long life is not random: it reflects measurable biological advantages in inflammation control, immune strength, metabolic stability, and genetic architecture.
Its core message:
Extreme longevity is a biological signatureâdefined by specific biomarkers that protect against disease and aging well into the tenth and eleventh decades of life....
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bxzxobhi-1709
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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âThe Impact of New Drug
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âThe Impact of New Drug Launches on Longevity
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âThe Impact of New Drug Launches on Longevityâ is âThe Impact of New Drug Launches on Longevityâ is an econometric and public-health analysis that quantifies how the introduction of new pharmaceuticals contributes to increases in life expectancy, reductions in mortality, and economic value creation across countries.
The report uses large datasetsâinternational drug launch records, disease mortality statistics, and demographic trendsâto show that innovative medicines are one of the most powerful drivers of improved longevity worldwide.
Its central conclusion is clear:
Launching new drugs saves lives on a national scale.
Countries that adopt new medicines sooner experience greater increases in life expectancy.
Core Findings
1. New drug launches significantly increase life expectancy
The paper demonstrates that most of the gains in longevity over recent decades are explained by new pharmaceutical therapies introduced after 1980.
Key evidence shows:
Each new drug launch is associated with measurable declines in disease-specific mortality.
Countries with faster uptake of new drugs experience larger increases in life expectancy than those with slower adoption.
Examples include:
New cardiovascular drugs reducing deaths from heart attacks and stroke
Oncology drugs lowering cancer mortality
HIV antiretroviral therapies increasing survival dramatically
2. âPharmaceutical innovationâ predicts mortality decline
The report uses time-series and cross-country regressions to show that:
The number of new drugs launched in a country strongly predicts the reduction of deaths in that country over the following years.
Older drugs have diminishing returns; most life-saving impact comes from new mechanisms, new molecular structures, and new therapeutic classes.
3. Drug innovation explains a large share of recent longevity growth
The analysis shows that new drugs account for:
A substantial percentage of the increase in life expectancy since the 1990s
A major portion of the decline in early-death years (years of life lost)
A large share of improvements in quality-adjusted life years (QALYs)
In some models, up to 70% of mortality reduction in major diseases is attributable to modern pharmaceutical innovation.
4. Countries adopting drugs later benefit less
The paper shows clear international disparities:
Countries that delay market approval for new drugs experience slower declines in mortality.
Regulatory speed and drug reimbursement policies directly influence national health outcomes.
This highlights the critical public-policy importance of faster approval, uptake, and access.
5. New drugs are cost-effective investments
The paper examines economic impacts and concludes that:
Although new drugs increase short-term spending,
They generate far greater long-term economic benefits via reduced hospitalization, reduced disability, and increased lifetime earnings.
Every dollar spent on pharmaceutical innovation yields multiple dollars in societal benefit through:
Improved survival
Higher labor productivity
Lower long-term medical costs
6. The largest longevity gains come from four therapeutic areas
Based on mortality-improvement models, the strongest life-extension effects arise from:
Cardiovascular drugs (statins, blood-pressure therapies, anticoagulants)
Oncology drugs
Infectious-disease therapies (HIV, hepatitis, vaccines)
CNS drugs (stroke recovery, neurodegeneration treatments)
These correspond to the biggest contributors to early mortality in industrialized nations.
Methodological Contributions
The paper uses:
International datasets from multiple decades
Drug launch timelines
Disease-specific mortality models
Country-fixed effects and year-fixed effects
Validation through both disease-level and aggregate analysis
This gives the findings strong statistical credibility and global relevance.
Conclusion
âThe Impact of New Drug Launches on Longevityâ demonstrates that pharmaceutical innovation is one of the most powerful forces increasing global life expectancy. New medicines reduce premature mortality across nearly all major disease categories, providing massive health and economic benefits to societies.
The reportâs message is definitive:
If countries want longer, healthier lives for their populations,
they must prioritize access to new, innovative medicines....
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