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Biological Age

anti-aging

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#151 VP.

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Posted 02 April 2019 - 04:16 PM

If they won't publish results from their research I can't consider using them. It's too bad because it looks promising. They don't answer my messages so that's not a good sign. 



#152 QuestforLife

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Posted 03 April 2019 - 08:05 AM

If they won't publish results from their research I can't consider using them. It's too bad because it looks promising. They don't answer my messages so that's not a good sign. 

 

If you go on their website and click on the chat icon you can talk in real time with a knowledgeable member of the team, which is what I did. They may have published, I don't know - but even if they haven't, it's no different to MyDNAge, who use propriety methylation sites.


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#153 albedo

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Posted 03 April 2019 - 08:57 AM

If you go on their website and click on the chat icon you can talk in real time with a knowledgeable member of the team, which is what I did. They may have published, I don't know - but even if they haven't, it's no different to MyDNAge, who use propriety methylation sites.

Yes, that could be a good approach. I also did a small search on co-founders such as Dr. Stubbs and Dr. Reik and found this work, a bit dated though (2017), which I will read: https://genomebiolog...017-1203-5#Sec8



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#154 VP.

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Posted 03 April 2019 - 09:06 PM

If you go on their website and click on the chat icon you can talk in real time with a knowledgeable member of the team, which is what I did. They may have published, I don't know - but even if they haven't, it's no different to MyDNAge, who use propriety methylation sites.

I had a chat with Toby from Chronomics about what test they used for biological age. I asked if the used the older Horvath test or pehaps the new GrimAge test and this was his answer:

 

We build our own more accurate predictor of biological age, drawing on genome wide sequencing data rather than methyl arrays

 

 

I did not get an answer whether their test is published yet or  if it has been submitted. 


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#155 VP.

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Posted 04 April 2019 - 02:50 PM

I had a chat with Toby from Chronomics about what test they used for biological age. I asked if the used the older Horvath test or pehaps the new GrimAge test and this was his answer:

 

 

 

I did not get an answer whether their test is published yet or  if it has been submitted. 

I talked some more to Toby and he said papers have been submitted on their research. 



#156 albedo

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Posted 20 April 2019 - 11:24 AM

https://gero.ai/bioage

(did not use it yet)



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#157 albedo

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Posted 26 May 2019 - 06:28 PM

The following is a highly recommended review paper by Claudio Franceschi, an extremely prolific author on aging, creator of the "inflammaging" theory of aging and leader of many studies, also large ones funded by EU as NU-AGE, particularly on the models represented by centenarians where more recently he and his team focused on the gut microbiome.

 

The paper touches many of the topics investigated in this Forum and aging theories. The link to this particular thread being the digression on biological age and relative biomarkers, in particular: DNA metylation, N-glycans and gut microbiota profiling.

 

Franceschi C, Garagnani P, Morsiani C, et al. The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates. Front Med (Lausanne). 2018;5:61.

 

"Geroscience, the new interdisciplinary field that aims to understand the relationship between aging and chronic age-related diseases (ARDs) and geriatric syndromes (GSs), is based on epidemiological evidence and experimental data that aging is the major risk factor for such pathologies and assumes that aging and ARDs/GSs share a common set of basic biological mechanisms. A consequence is that the primary target of medicine is to combat aging instead of any single ARD/GSs one by one, as favored by the fragmentation into hundreds of specialties and sub-specialties. If the same molecular and cellular mechanisms underpin both aging and ARDs/GSs, a major question emerges: which is the difference, if any, between aging and ARDs/GSs? The hypothesis that ARDs and GSs such as frailty can be conceptualized as accelerated aging will be discussed by analyzing in particular frailty, sarcopenia, chronic obstructive pulmonary disease, cancer, neurodegenerative diseases such as Alzheimer and Parkinson as well as Down syndrome as an example of progeroid syndrome. According to this integrated view, aging and ARDs/GSs become part of a continuum where precise boundaries do not exist and the two extremes are represented by centenarians, who largely avoided or postponed most ARDs/GSs and are characterized by decelerated aging, and patients who suffered one or more severe ARDs in their 60s, 70s, and 80s and show signs of accelerated aging, respectively. In between these two extremes, there is a continuum of intermediate trajectories representing a sort of gray area. Thus, clinically different, classical ARDs/GSs are, indeed, the result of peculiar combinations of alterations regarding the same, limited set of basic mechanisms shared with the aging process. Whether an individual will follow a trajectory of accelerated or decelerated aging will depend on his/her genetic background interacting lifelong with environmental and lifestyle factors. If ARDs and GSs are manifestations of accelerated aging, it is urgent to identify markers capable of distinguishing between biological and chronological age to identify subjects at higher risk of developing ARDs and GSs. To this aim, we propose the use of DNA methylation, N-glycans profiling, and gut microbiota composition to complement the available disease-specific markers."



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#158 VP.

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Posted 05 June 2019 - 02:30 PM

Strait from Steve Horvath: 

Rapamycin retards epigenetic ageing of keratinocytes independently of its effects on replicative senescence, proliferation and differentiation

 

The advent of epigenetic clocks has prompted questions about the place of epigenetic ageing within the current understanding of ageing biology. It was hitherto unclear whether epigenetic ageing represents a distinct mode of ageing or a manifestation of a known characteristic of ageing. We report here that epigenetic ageing is not affected by replicative senescencetelomere length, somatic cell differentiation, cellular proliferation rate or frequency. It is instead retarded by rapamycin, the potent inhibitor of the mTOR complex which governs many pathways relating to cellular metabolism. Rapamycin, however, is also an effective inhibitor of cellular senescence. Hence cellular metabolism underlies two independent arms of ageing – cellular senescence and epigenetic ageing. The demonstration that a compound that targets metabolism can slow epigenetic ageing provides a long-awaited point-of-entry into elucidating the molecular pathways that underpin the latter. Lastly, we report here an in vitro assay, validated in humans, that recapitulates human epigenetic ageing that can be used to investigate and identify potential interventions that can inhibit or retard it.

In summary, the observations above represent the first biological connection between epigenetic ageing and rapamycin. These results for human cells add to the evidence that extension of life, at least by rapamycin, is indeed accompanied by retardation of ageing. These observations also suggest that the life-extending property of rapamycin may be a resultant of its multiple actions which include, but not necessarily limited to suppression of cellular senescence [3638,48] and epigenetic aging, with the possibility of augmentation of cellular proliferative potential.

 

https://www.aging-us...cle/101976/text







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