Three Tiers to biological escape velocity: The quest to outwit aging

Probably not a substantial claim. The paper’s conclusions may not depend on it.

Homo sapiens evolved from a diverse range of random gene mutations over hundreds of millions of years.

“Homo sapiens evolved from a diverse range of random gene mutations over a period of hundreds of millions of years, 9”

• cites [9] Lopez‐Bigas N, De S, Teichmann SA. Functional protein divergence in the evolution of Homo sapiens. Genome Biol. 2008; 9(2): R33. doi: 10.1186/GB-2008-9-2-R33 18279504 PMC2374701 sourcePartly supported

  The Background (page not provided) describes a history of mutations and selection leading to the human lineage, and the Discussion describes differing rates of protein-coding gene divergence. The paper does not characterize those mutations as random or state that Homo sapiens evolved over hundreds of millions of years. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim. The paper’s conclusions may not depend on it.

Particular gut microbiota are associated with neuroinflammation resulting in the pathogenesis of Alzheimer's disease.

“Chen et al. recently demonstrated that particular gut microbiota are associated with neuroinflammation resulting in the pathogenesis of Alzheimer's disease. 46”

• cites [46] Chen C, Liao J, Xia Y, et al. Gut microbiota regulate Alzheimer's disease pathologies and cognitive disorders via PUFA‐associated neuroinflammation. Gut. 2022; 71: 2233‐ 2252. doi: 10.1136/GUTJNL-2021-326269 35017199 PMC10720732 sourceSupported

It may state two separate claims as one.

17α-estradiol extends life in male mice by 19% but has no effect in female mice.

“17α‐estradiol (17α‐E2), a weak endogenous steroidal estrogen that is also a nonfeminizing version of estradiol, has been shown to extend life in male mice by 19% but did not show any effect in female mice. 11”

• cites [11] Strong R, Miller RA, Antebi A, et al. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an α‐glucosidase inhibitor or a Nrf2‐inducer. Aging Cell. 2016; 15(5): 872‐ 884. doi: 10.1111/ACEL.12496 27312235 PMC5013015 sourceSupported

It may state two separate claims as one.

Eotaxin increases with age and negative regulation should be a key target for healthy aging.

“Eotaxin is known to increase with age and negative regulation should be a key target for healthy aging. 68”

• cites [68] Hoefer J, Luger M, Dal‐Pont C, et al. The ‘aging factor’ eotaxin‐1 (CCL11) is detectable in transfusion blood products and increases with the donor's age. Front Aging Neurosci. 2017; 9: 402. doi: 10.3389/FNAGI.2017.00402/BIBTEX 29249965 PMC5717008 sourcePartly supported

  The Discussion reports that eotaxin-1 rises significantly with donor age, supporting the first part of the claim. The Introduction and Discussion link elevated eotaxin-1 to impaired neurogenesis and cognition, but do not say that reducing it should be a key target for healthy aging. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

It may state two separate claims as one.

Evolutionary escape velocity has already been reached with Tier 3 technologies, with the human species no longer requiring gene mutations over thousands of years to become stronger or healthier.

“Evolutionary escape velocity has already been reached with Tier 3 technologies, with the human species no longer requiring gene mutations over the course of thousands of years to become stronger or healthier as technologies to edit genes are already here. 56”

• cites [56] Loewe L, Hill WG. The population genetics of mutations: good, bad and indifferent. Philos Trans R Soc B Biol Sci. 2010; 365(1544): 1153‐ 1167. doi: 10.1098/RSTB.2009.0317 PMC2871823 20308090 sourceCould not verify

  The introduction (p. 1) describes mutations as raw materials for evolution, and General Questions and Applications (p. 11) discusses their role in adaptation. Searches for “evolutionary escape velocity,” “Tier 3 technologies,” and human gene editing found no passage addressing whether technology has removed the need for mutations over thousands of years. (LLM, conf=0.76)

  Experimental — accuracy not yet measured

It may state two separate claims as one.

CRISPR Cas9, Base and Prime editing, PASTE, and other versions of gene editing are becoming cost effective and may become mainstream services accessible to the general public.

“CRISPR Cas9, Base and Prime editing, Programmable Addition via Site‐specific Targeting Elements (PASTE), and other versions of gene editing are becoming cost effective and may cause the trajectory of these technologies to become mainstream services that the general public can access easily. 48 , 50 , 51”

• cites [48] Wareham CS. Genome editing for longer lives: the problem of loneliness. J Bioeth Inq. 2020; 17(2): 309‐ 314. doi: 10.1007/S11673-020-09967-W 32152896Not checked yet
• cites [50] Kantor A, McClements ME, Maclaren RE. CRISPR‐Cas9 DNA Base‐editing and prime‐editing. Int J Mol Sci. 2020; 21(17): 1‐ 22. doi: 10.3390/IJMS21176240 PMC7503568 32872311 sourcePartly supported

  The Introduction and Conclusions discuss CRISPR-Cas9, base editing, and prime editing and describe their therapeutic potential. They do not support the claims that these technologies are becoming cost-effective or may become easily accessible mainstream services for the general public; the passages found also do not discuss PASTE. The Conclusions instead emphasize that safe, effective delivery remains a major hurdle. (LLM, conf=0.84)

  Experimental — accuracy not yet measured
• cites [51] Hosur V, Low BE, Wiles MV. Programmable RNA‐guided large DNA transgenesis by CRISPR/Cas9 and site‐specific integrase Bxb1. Front Bioeng Biotechnol. 2022; 10: 1. doi: 10.3389/FBIOE.2022.910151 PMC9294445 35866031 sourcePartly supported

  The sections on PASTE and Conclusion and Future Directions discuss PASTE, CRISPR-Cas9, base editing, and prime editing. But Available Tools: Strengths and Weaknesses calls the lack of economical techniques for precise large-DNA integration a key obstacle; the paper does not say these technologies are becoming cost-effective or may become easily accessible mainstream services for the general public. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

It may state two separate claims as one.

No other therapy currently discussed in the paper can rewind aged tissues, but Yamanaka Factors appear promising as a first step in rewinding biological time.

“Whilst no other therapy currently discussed in this paper can rewind aged tissues, Yamanaka Factors appear promising in what could be a first step in rewinding biological time”

• cites [53] Rando TA, Chang HY. Aging, rejuvenation, and epigenetic reprogramming: resetting the aging clock. Cell. 2012; 148(1–2) NIH Public Access: 46‐ 57. doi: 10.1016/j.cell.2012.01.003 22265401 PMC3336960 sourcePartly supported

  The ‘Resetting of the Aging Clock’ section says iPSC generation rewinds the aging clock, supporting the idea that Yamanaka-factor reprogramming is a promising starting point. But it also says this process removes cells’ differentiated identity and may be harmful if applied to aged tissues; it does not establish a therapy that rewinds aged tissues. The ‘no other therapy’ comparison concerns the citing paper’s own discussion, not a comparison this source can verify. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

Probably not a substantial claim.

Tier 2 captures full spectrum biological surveillance looking at the entire human biological condition.

“Tier 2 captures full spectrum biological surveillance looking at the entire human biological condition”

• cites [32] Horvath S. DNA methylation age of human tissues and cell types. Genome Biol. 2013; 14(10): R115. doi: 10.1186/gb-2013-14-10-r115 24138928 PMC4015143 sourceNot checked yet
• cites [33] Carrozza MJ, Utley RT, Workman JL, Côté J. The diverse functions of histone acetyltransferase complexes. Trends Genet. 2003; 19(6) Elsevier Ltd: 321‐ 329. doi: 10.1016/S0168-9525(03)00115-X 12801725 sourceNot checked — no full text of the source
• cites [34] Shammas MA. Telomeres, lifestyle, cancer, and aging. Curr Opin Clin Nutr Metab Care. 2011; 14(1): 28‐ 34. doi: 10.1097/MCO.0b013e32834121b1 21102320 PMC3370421Not checked yet

Probably not a substantial claim. The paper may give no reason why it holds.

There are three clear classes (Tiers) of longevity systems currently under development.

“This discussion finds that there are three clear classes (Tiers) of longevity systems that are currently under development”

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.

Tier 1 interventions are noninvasive, relatively simple for end users, and mostly cost effective.

“These Tier 1 interventions remain noninvasive, relatively simple for end users, and mostly cost effective.”

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.

Much of Tier 2 is already available across the world for those willing to take preemptive action.

“Much of Tier 2 is already available across the world for those willing to take preemptive action”

It may state two separate claims as one.

DGLA can disrupt cellular lipid metabolism, including eicosanoid biosynthesis, and may slow cell division and increase lifespan.

“DGLA is able to disrupt cellular lipid metabolism, including eicosanoid biosynthesis that (through its antiproliferation effects) may be able to slow down cell division and increase lifespan.”

• cites [29] Pietzner M, Stewart ID, Raffler J, et al. Multiple roles of dihomo‐γ‐linolenic. Nat Med. 2021; 27(3): 471‐ 479. doi: 10.1038/s41591-021-01266-0 33707775 PMC8127079Not checked yet
• cites [30] Kernoff PBA, Willis AL, Stone KJ, Davies JA, Mcnicol GP. Antithrombotic potential of dihomo‐gamma‐linolenic acid in man. Br Med J. 1977; 2(6100): 1441‐ 1444. doi: 10.1136/BMJ.2.6100.1441 338112 PMC1632618Not checked yet

Probably not a substantial claim. The paper may give no reason why it holds.

Knowing mortality prediction data allows a subject to take evasive action.

“Knowing this type of confronting data (mortality prediction) allows a subject to take evasive action.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.

Full spectrum surveillance is an extremely powerful approach in human health and longevity, as preventative medicine now makes it possible to prevent disease before it starts.

“Full spectrum surveillance is clearly an extremely powerful approach in human health and longevity, as preventative medicine now makes it possible to prevent disease before it starts.”

• AssumptionRests on an assumption: Most if not all humans will have a predisposition to some disease at some stage.
• AssumptionRests on an assumption: Disease predispositions dormant in human genes can be found years before they happen and many can be defused with various interventions.

Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

Nanoparticles can deliver hydrophilic and hydrophobic therapeutic agents, enhance absorption, protect molecules from stomach acids, and reduce toxic side effects.

“nanoparticles have the ability to deliver hydrophilic and hydrophobic therapeutic agents, enhance absorption, protect various molecules from stomach acids, and reduce toxic side effects. 27 , 28”

• cites [27] Shade CW. Liposomes as advanced delivery Systems for Nutraceuticals. Integr Med A Clin J. 2016; 15(1): 33 Accessed October 28, 2022. [Online]. Available: /pmc/articles/PMC4818067/. PMC4818067 27053934Not checked yet
• cites [28] Davis JL, Paris HL, Beals JW, et al. Liposomal‐encapsulated ascorbic acid: Influence on vitamin C bioavailability and capacity to protect against ischemia–reperfusion injury. Nutr Metab Insights. 2016; 9: 25‐ 30. doi: 10.4137/NMI.S39764 27375360 PMC4915787 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

It may state two separate claims as one.

Tier 1 interventions are unable to predict disease, prevent genomic mutations, or regulate profound gene activity to prevent the onset of age.

“However, Tier 1 interventions are unable to predict disease, prevent genomic mutations, or regulate profound gene activity to prevent the onset of age.”

It may state two separate claims as one.

Inhibition of NNMT activates senescent muscle stem cells and improves rejuvenation capacity of aged skeletal muscle.

“Inhibition of NNMT has also been shown to activate senescent muscle stem cells and the rejuvenation capacity of aged skeletal muscle. 15”

• cites [15] Neelakantan H, Brightwell CR, Graber TG, et al. Small molecule nicotinamide N‐methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019; 163: 481‐ 492. doi: 10.1016/J.BCP.2019.02.008 30753815 PMC6469996 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

Probably not a substantial claim.

Tier 2 functions as the disease prediction and prevention phase.

“Tier 2 functions as the disease prediction and prevention phase.”

• AssumptionRests on an assumption: Most if not all humans will have a predisposition to some disease at some stage.
• AssumptionRests on an assumption: Disease predispositions dormant in human genes can be found years before they happen and many can be defused with various interventions.

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.

Tier 2 therapies are focused on investigative and preventative diagnostics, including full body MRIs, electrocardiograms, pathology, and glycomic, genetic, and methylation screening.

“Tier 2 therapies are focused on investigative and preventative diagnostics. Full body MRIs, electrocardiograms, pathology, and glycomic, genetic, and methylation screening are all part of Tier 2 treatments.”

Probably not a substantial claim. The paper may give no reason why it holds.

Many drivers of the aging process can now be modified with simple Tier 1 interventions.

“Many drivers of the aging process can now be modified with simple Tier 1 interventions.”

Probably not a substantial claim. The paper may give no reason why it holds.

All three Tiers are paramount to achieve biological escape velocity, where tissues can be repaired faster than aging can damage them.

“all three will be paramount to achieve biological escape velocity (where tissues can be repaired faster than aging can damage them).”

Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.

Challenges to collate deep Tier 2 data remain elusive to commercialization and most likely require powerful AI to process.

“the challenges to collate this type of deep data remains elusive to commercialization and that it most likely requires powerful artificial intelligence (AI) to process such an overwhelming amount of data”

It may state two separate claims as one.

DGLA shows promise in healthy aging as an antiinflammatory, antithrombotic, and antiproliferation approach for disease, notably cancer.

“Dihomo‐γ‐linolenic acid (DGLA) is also showing great promise in healthy aging as an antiinflammatory, antithrombotic, and an antiproliferation approach for disease, notably cancer. 29 , 30”

• cites [29] Pietzner M, Stewart ID, Raffler J, et al. Multiple roles of dihomo‐γ‐linolenic. Nat Med. 2021; 27(3): 471‐ 479. doi: 10.1038/s41591-021-01266-0 33707775 PMC8127079Not checked yet
• cites [30] Kernoff PBA, Willis AL, Stone KJ, Davies JA, Mcnicol GP. Antithrombotic potential of dihomo‐gamma‐linolenic acid in man. Br Med J. 1977; 2(6100): 1441‐ 1444. doi: 10.1136/BMJ.2.6100.1441 338112 PMC1632618Not checked yet

Probably not a substantial claim. The paper’s conclusions may not depend on it.

Activation of NRF2 is a target for longevity researchers because its function offers therapeutic potential for oxidative stress or inflammation diseases including neurodegenerative, metabolic, and cardiovascular diseases.

“Activation of NRF2 is now a target for longevity researchers as its function offers therapeutic potential for numerous diseases that involve oxidative stress or inflammation including neurodegenerative, metabolic, and cardiovascular diseases.”

• cites [19] Robledinos‐Antón N, Fernández‐Ginés R, Manda G, Cuadrado A. Activators and inhibitors of NRF2: a review of their potential for clinical development. Oxid Med Cell Longev. 2019; 2019: 1‐ 20. doi: 10.1155/2019/9372182 PMC6664516 31396308 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

It may state two separate claims as one.

Telomerase induction therapies, restorative proteomic therapies, and prevention of genomic instability are emerging technologies that can assist in maintaining youthful tissue function.

“Sophisticated interventions such as telomerase induction therapies, 43 restorative proteomic therapies to rejuvenate tissues, 44 and prevention of genomic instability 45 are among emerging technologies that can assist in maintaining youthful tissue function.”

• cites [43] Saretzki G. Telomeres, telomerase and ageing. Subcell Biochem. 2018; 90: 221‐ 308. doi: 10.1007/978-981-13-2835-0_9 30779012Not checked yet
• cites [44] North BJ, Rosenberg MA, Jeganathan KB, et al. Sirt2OEで寿命延長 チェックポイントキナーゼであるBubR1を介している SIRT2 induces the checkpoint kinase BubR1 to increase lifespan. EMBO J. 2014; 33(13): 1438‐ 1453. 24825348 PMC4194088 sourceNot checked yet
• cites [45] Langie SAS, Koppen G, Desaulniers D, et al. Causes of genome instability: the effect of low dose chemical exposures in modern society. Carcinogenesis. 2015; 36(Suppl 1): S61‐ S88. doi: 10.1093/CARCIN/BGV031 26106144 PMC4565613Not checked yet

It may state two separate claims as one.

Low serum DGLA levels are associated with mediocre health outcomes in myocardial infarction and increased risk of total death in elderly patients with MI.

“Low levels of serum DGLA are associated with mediocre health outcomes in myocardial infarction (MI) and an increased risk of total death in elderly patients with MI. 31”

• cites [31] Nilsen DWT, Myhre PL, Kalstad A, Schmidt EB, Arnesen H, Seljeflot I. Serum levels of Dihomo‐gamma (γ)‐linolenic acid (DGLA) are inversely associated with linoleic acid and Total death in elderly patients with a recent myocardial infarction. Nutrients. 2021; 13(10): 3475. doi: 10.3390/NU13103475 34684479 PMC8540726Not checked yet

Probably not a substantial claim. The paper’s conclusions may not depend on it.

Some genes deliver disease or aging.

“some genes deliver disease or aging. 10”

• cites [10] Rodríguez‐Rodero S, Fernández‐Morera JL, Menéndez‐Torre E, Calvanese V, Fernández AF, Fraga MF. Aging genetics and aging. Aging Dis. 2011; 2(3): 186 Accessed July 7, 2021. [Online]. Available: /pmc/articles/PMC3295054/. 22396873 PMC3295054Not checked — no full text of the source

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.

Tier 1 interventions are relatively easy to implement, cost effective, and noninvasive.

“This paper will show that Tier 1 interventions are relatively easy to implement as they remain cost effective and noninvasive, with the most challenging part simply being able to change behaviors that relate to diet or refraining from eating during fasting periods.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.

Inferior genomes look set to be edited out with technologies such as CRISPR-Cas9, PASTE, or base and prime editing, and this control over natural selection is evolutionary escape velocity, whereas repairing tissues faster than aging can destroy them is biological escape velocity.

“Inferior genomes look set to be edited out with technologies such as CRISPR‐Cas9, PASTE, or base and prime editing, and this control over natural selection is evolutionary escape velocity, whereas repairing tissues faster than aging can destroy them is biological escape velocity.”

Probably not a substantial claim. The paper’s conclusions may not depend on it.

Gene and epigenetic silencing such as CRISPR DCas9 are options for consumers apprehensive about full gene editing.

“Gene and epigenetic silencing such as CRISPR DCas9 are also options that may be considered for those consumers apprehensive about full gene editing. 52”

• cites [52] Depardieu F, Bikard D. Gene silencing with CRISPRi in bacteria and optimization of dCas9 expression levels. Methods. 2020; 172: 61‐ 75. doi: 10.1016/J.YMETH.2019.07.024 31377338 sourceNot checked — no full text of the source

Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.

There are three distinct classes of longevity and anti-aging technologies emerging globally, and the ability of each class is apparent in fending off aspects of biological decay.

“This discussion evidently finds that there are three distinct classes of longevity and anti‐aging technologies that are emerging globally, and the ability of each class is clearly apparent in fending off aspects of biological decay.”

It may state two separate claims as one.

Human evolution on Earth functions by random gene mutations to ensure life forms evolve and adapt, and this process of natural selection takes thousands of years.

“Human evolution on Earth functions by random gene mutations to ensure life forms evolve and are adaptable to survive in their environment, though this process of natural selection takes thousands of years. 57 , 58”

• cites [57] Kleinman A. The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance. Stat Med. 2016; 35(29): 5391‐ 5400. doi: 10.1002/SIM.7070 27501057 PMC6175190Not checked yet
• cites [58] Mutations Are the Raw Materials of Evolution | Learn Science at Scitable. Accessed July 29, 2022. https://www.nature.com/scitable/knowledge/library/mutations‐are‐the‐raw‐materials‐of‐evolution‐17395346/Not checked yet

It may state two separate claims as one.

Restoring various serum proteins back into the blood will become a major target to restore youthful function into aged tissues, and beneficial proteins with rejuvenation properties include IGF2, GHRH, GnRH, and GDF11.

“Restoring various serum proteins back into the blood will become a major target to restore youthful function back into aged tissues, and there are many beneficial proteins that hold rejuvenation properties such as insulin growth factor two (IGF2), 60 , 61 growth hormone releasing hormone ((GHRH), 62 gonadotropin releasing hormone GnRH), 63 and growth differentiation factor 11 (GDF11). 64 , 65”

• cites [60] Stern SA, Chen DY, Alberini CM. The effect of insulin and insulin‐like growth factors on hippocampus‐ and amygdala‐dependent long‐term memory formation. Learn Mem. 2014; 21(10): 556‐ 563. doi: 10.1101/LM.029348.112 25227250 PMC4175499 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

• cites [62] Friedman SD, Baker LD, Borson S, et al. Growth hormone‐releasing hormone effects on brain γ‐aminobutyric acid levels in mild cognitive impairment and healthy aging. JAMA Neurol. 2013; 70(7): 883‐ 890. doi: 10.1001/JAMANEUROL.2013.1425 23689947 PMC3764915 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

• cites [64] Idkowiak‐Baldys J, Santhanam U, Buchanan SM, et al. Growth differentiation factor 11 (GDF11) has pronounced effects on skin biology. PLoS One. 2019; 14(6): e0218035. doi: 10.1371/JOURNAL.PONE.0218035 31181098 PMC6557520 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

It may state two separate claims as one.

β2-microglobulin is a pro-aging factor that contributes to impaired cognition and improper neurogenesis.

“β2‐microglobulin, which is considered a pro‐aging factor that also contributes to impaired cognition and improper neurogenesis. 69”

• cites [69] Smith LK, He Y, Park JS, et al. β2‐microglobulin is a systemic pro‐aging factor that impairs cognitive function and neurogenesis. Nat Med. 2015; 21(8): 932‐ 937. doi: 10.1038/NM.3898 26147761 PMC4529371 sourceNot checked yet

It may state two separate claims as one.

Tissue reprogramming with Yamanaka Factors is well underway and may allow aged organisms to rejuvenate organs and tissues in vivo.

“Tissue reprogramming with Yamanaka Factors is also well underway and may allow aged organisms to rejuvenate their organs and tissues in vivo. 53”

• cites [53] Rando TA, Chang HY. Aging, rejuvenation, and epigenetic reprogramming: resetting the aging clock. Cell. 2012; 148(1–2) NIH Public Access: 46‐ 57. doi: 10.1016/j.cell.2012.01.003 22265401 PMC3336960 sourceNot checked yet

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.

Altering genes, epigenetic expression, cellular reprogramming, and systemic tissue rejuvenation is coming to mainstream health and medicine soon.

“Altering genes, epigenetic expression, cellular reprogramming, and systemic tissue rejuvenation is certainly coming to mainstream health and medicine soon.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.

No matter what a subject's genome, superior or inferior, the natural evolutionary pathway is soon to be redundant.

“No matter what a subject's genome, superior or inferior, the natural evolutionary pathway is soon to be redundant.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.

Tier 3 reigns supreme in rejuvenation therapies that may make up future pathways to reach biological escape velocity.

“Tier 3, however, reigns supreme in rejuvenation therapies that may make up future pathways to reach biological escape velocity.”

Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.

Humans now control how their species will age and evolve.

“Humans now control how their species will age and evolve.”

Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.

mRNA may be more palatable to commercial services as it does not require gene editing and can induce healthy protein function in subjects with single nucleotide polymorphisms for a particular protein.

“mRNA may also be more palatable to commercial services as it does not require gene editing and can induce healthy protein function in subjects that may even have single nucleotide polymorphisms for a particular protein, thus bypassing the body's need for transcription of that faulty gene.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.

The Tier 3 technologies used to achieve biological escape velocity indicate that the death of human natural selection is here.

“The Tier 3 technologies used to achieve biological escape velocity clearly indicate that the death of human natural selection is here”

It may state two separate claims as one.

Tier 3 treatments remain expensive and elusive but are already emerging onto the world stage.

“Tier 3 treatments remain expensive and elusive but are already emerging onto the world stage.”

It may state two separate claims as one.

Eotaxin is correlated with many neurological conditions (neurodegenerative, neuroinflammatory, and neuropsychiatric disorders), earning names ECDC or ABAC.

“Because eotaxin is correlated with so many neurological conditions (neurodegenerative, neuroinflammatory, and neuropsychiatric disorders), it has earned the name “Endogenous Cognition Deteriorating Chemokine” (ECDC) or “Accelerated Brain‐Aging Chemokine” (ABAC). 67”

• cites [67] Ivanovska M, Abdi Z, Murdjeva M, Macedo D, Maes A, Maes M. CCL‐11 or Eotaxin‐1: an immune marker for ageing and accelerated ageing in neuro‐psychiatric disorders. Pharmaceuticals. 2020; 13(9): 1‐ 17. doi: 10.3390/PH13090230 PMC7558796 32887304 sourceNot checked yet

  Checked before — its earlier verdict is held back until a new check runs.

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.

For the first time Homo sapiens are taking control of evolution and aging, as techniques that will overcome aging are within grasp.

“For the first time Homo sapiens are taking control of evolution and aging, as the techniques that will overcome aging are now within grasp.”

It may state two separate claims as one.

Proteins implicated in age-related decline such as eotaxin and β2-microglobulin must be managed, otherwise healthy aging cannot be achieved effectively.

“These types of proteins (eotaxin and β2‐microglobulin) that are implicated in age‐related decline must be managed, otherwise healthy aging cannot be achieved effectively.”

• AssumptionRests on an assumption: Disease predispositions dormant in human genes can be found years before they happen and many can be defused with various interventions.

It may state two separate claims as one.

Differences in individual methylation status and biological age mean cellular reprogramming will never be a one size fits all, as rewinding cells too far back could have dire consequences for specific tissues.

“differences in an individual's methylation status and biological age sees that cellular reprogramming will never be a one size fits all, as rewinding cells too far back could have dire consequence for specific tissues. 53 , 54 , 55”

• cites [53] Rando TA, Chang HY. Aging, rejuvenation, and epigenetic reprogramming: resetting the aging clock. Cell. 2012; 148(1–2) NIH Public Access: 46‐ 57. doi: 10.1016/j.cell.2012.01.003 22265401 PMC3336960 sourceNot checked yet
• cites [54] Zhang Y‐X, Chen S‐L, Li Y‐M, Zheng Y‐W. Limitations and challenges of direct cell reprogramming in vitro and in vivo. Histol Histopathol. 2022; 37: 18458. doi: 10.14670/HH-18-458 35417038Not checked yet
• cites [55] Tobe BTD, Brandel MG, Nye JS, Snyder EY. Implications and limitations of cellular reprogramming for psychiatric drug development. Exp Mol Med. 2013; 45(11): e59. doi: 10.1038/EMM.2013.124 24232258 PMC3849573Not checked yet

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.

Reducing serum proteins that appear to induce age-related disease is paramount for tissue engineering therapies.

“Moreover, reducing other serum proteins that appear to induce age‐related disease would also be paramount in seeing tissue engineering therapies successful.”

Probably not a substantial claim. The paper’s conclusions may not depend on it.

Numerous companies are now pursuing genetic engineering to achieve longevity by maintaining tissue vibrancy, disease resistance, and organismal vitality.

“Numerous companies are now pursuing genetic engineering to achieve longevity by maintaining tissue vibrancy, disease resistance, and organismal vitality. 48”

• cites [48] Wareham CS. Genome editing for longer lives: the problem of loneliness. J Bioeth Inq. 2020; 17(2): 309‐ 314. doi: 10.1007/S11673-020-09967-W 32152896Not checked yet

It may state two separate claims as one.

The human race has now devised ways to ensure that inferior genomes no longer cause early mortality or are passed down to offspring.

“The human race has now devised ways to ensure that inferior genomes no longer cause early mortality or are passed down to their offspring.”

Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.

Unborn babies that exhibit a disease phenotype may now be genetically edited and no longer born weak with little chance of survival; natural selection has changed forever with Tier 3 technologies.

“Unborn babies that exhibit a disease phenotype may now be genetically edited and no longer will they be born weak with little chance of survival; natural selection has changed forever with Tier 3 technologies.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.

Humans have power over their default gene configuration to ensure genes can be edited at will, and if tissues can be rejuvenated faster than aging can destroy them, then biological escape velocity is reached.

“Humans have the power over their default gene configuration to ensure that genes can be edited at will and if tissues can be rejuvenated faster than aging can destroy them, then we have reached another goal known as biological escape velocity.”

It may state two separate claims as one.

Due to Tier 2 diagnostics being time intensive, until AI can process the data, Tier 2 is likely to remain costly and only available from specialized clinics.

“Due to Tier 2 diagnostics being time intensive, until AI can process the vast wealth of data that full spectrum biological surveillance needs to generate, it is likely to remain costly and only available from specialized clinics.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.

The human body is genetic code, and reprogramming that code or adjusting proteins from that code allows power over human evolution and aging to be exerted.

“Ultimately the human body is genetic code, and simply reprogramming that code, or adjusting the proteins from that code, infers that power over human evolution and aging can be exerted.”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.

Biology can be changed and reprogrammed, and this is where the requirement for Tier 3 exists.

“biology can also be changed and reprogrammed, and this is where the requirement for Tier 3 exists.”

Probably not a substantial claim. The paper may give no reason why it holds.

Tier 3 technologies remain the only observable therapies that may be able to prevent aspects of aging and deliver rejuvenation of tissues faster than aging can damage those tissues.

“Tier 3 technologies remain the only observable therapies that may be able to prevent aspects of aging and deliver rejuvenation of tissues faster than aging can damage those tissues (Figure 1).”

Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.

Without Tier 2 insight, subjects wishing to maintain healthy physiology are blinded to dangers hidden inside their biology.

“Without Tier 2 insight, subjects wishing to maintain healthy physiology are simply blinded to any dangers hidden inside their biology.”

• AssumptionRests on an assumption: Most if not all humans will have a predisposition to some disease at some stage.

It may state two separate claims as one.

Many genes are already identified as aging genes or youth genes, and modifying their expression or existence will hold profound downstream impacts for lifespan.

“Many genes are already identified as aging genes or youth genes10, 49 and modifying the expression or existence of these genes will hold profound downstream impacts for lifespan.”

• cites [10] Rodríguez‐Rodero S, Fernández‐Morera JL, Menéndez‐Torre E, Calvanese V, Fernández AF, Fraga MF. Aging genetics and aging. Aging Dis. 2011; 2(3): 186 Accessed July 7, 2021. [Online]. Available: /pmc/articles/PMC3295054/. 22396873 PMC3295054Not checked — no full text of the source
• cites [49] Di CC, Zeldich E, Li Y, Yuste A, Abraham CR. Activation of the anti‐aging and cognition‐enhancing gene klotho by CRISPR‐dCas9 transcriptional effector complex. J Mol Neurosci. 2018; 64(2): 175‐ 184. doi: 10.1007/s12031-017-1011-0 29352444 PMC5826803Not checked yet