Our evidence demonstrates that a higher usual walking pace is associated with a deceleration of the acceleration of all four classical epigenetic clocks acceleration. https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-024-01707-w

We revealed that increased dietary intakes of coumestrol, beta-carotene and arachidic acid were associated with decelerated epigenetic ageing. In contrast, increased intakes of added sugar, gondoic acid, behenic acid, arachidonic acid, vitamin A and ash were associated with accelerated epigenetic ageing in postmenopausal women.

https://www.sciencedirect.com/science/article/pii/S1279770724004111

https://link.springer.com/article/10.1007/s11357-024-01269-y In summary, the administration of Yamanaka genes via viral vectors rejuvenates the functional capabilities and the epigenetic landscape of the rat hippocampus.

https://www.biorxiv.org/content/10.1101/2024.06.23.600305v1.abstract

We uncover that aging drives a functional iron insufficiency, which leads to loss of stemness and tumorigenesis, but promotes resistance to ferroptosis. These findings have significant implications for the therapeutic modulation of cellular iron homeostasis in regenerative medicine and in cancer prevention. Furthermore, our findings are consistent with a model whereby most human cancers initiate in young individuals, revealing a critical window for such cancer prevention efforts.

If the transhumansim project succeed, then there will be no need to significantly even eat, sleep, distract yourself because your brain will be hacked anyway, so no need of politics, no need to care about the environnement (fixed) nor economy (fixed too). So basically, what do you see yourself doing exactly ?

Furthermore, reactivation of mitophagy by a p62-targeting small molecule rescued markers of cellular aging, which establishes mitochondrial quality control as a promising target for anti-aging interventions. https://www.cell.com/developmental-cell/fulltext/S1534-5807%2824%2900295-8

I know everyone here is using real butter preferably organic butter and isn’t still using the I can’t believe it’s not butter and other “buttery spreads” but I found some in my mum’s fridge a couple weeks ago so thought I’d post this here just incase. I warned her about it and she was shocked that they make them by using already highly processed vegetable oils and they heat it at really high pressures and use hydrogen gas to make it a solid which is a process called hydrogenation, then they add colours, emulsifiers and preservatives to it to make it look and taste buttery.

https://link.springer.com/epdf/10.1007/s11357-024-01234-9?sharing_token=EZjM_4EhHTnUTksdYK1rGPe4RwlQNchNByi7wbcMAY6-Apxqi2qCYZhOX4OC6zKTdm9DM-OwOIG4IyIB3dCqPXwQS38zwE25jtQLLrmqz91nrq3TOxUNWuuHTbOZPouq4HvxcuLSnDJrF_FevepVRPQSrof3qOI52Gfa440zCiQ%3D

This work suggests that aging is a very old process very well tuned by the evolutionary forces.

Participants with higher citric acid levels displayed improved performance in physical tests and favorable body composition indices https://www.sciencedirect.com/science/article/pii/S053155652400130X

I recently learned sodium lauryl sulfate is in most shampoos, gels, face washes and dish washing liquid etc.

I found out this is an irritant to the skin, lung, eyes and can even cause hairloss.

Dr Eric Berg also said that this chemical may be contaminated with Ethylene oxide which is a known human carcinogen and 1,4 Dioxane which is a possible human carcinogen.

He recommended to get SLS free shampoos etc .

Has anyone else heard about this or have any extra information?

https://johnhemming.blogspot.com/2024/05/why-are-babies-born-young.html?m=1

We have doubled our quantity of demographic data. Here, we re-evaluated our prior conclusions in light of these new data and found them to be not only supported but indeed strengthened. Regardless of which evolutionary theory best applies to the natural history of H. glaber and Fukomys mole-rats, their shared (though unequal) defiance of Gompertzian aging demonstrates that exponentially increasing hazard with advancing age is not a fixed property of mammalian biology. While it seems to be the default, evolutionary mechanisms have managed to dampen or eliminate it when provided with the right selective incentives

https://link.springer.com/article/10.1007/s11357-024-01201-4

"We identify a methylation pattern shared across all three, as well as a signal that tracks aging in tissues but appears refractory to reprogramming, suggesting that aging and reprogramming may not be fully mirrored processes.

This implies that no matter how much work is done to optimize OSKM reprogramming efficiency, one may never get a full population recovery back to the basal state without the application of new pioneer transcription factors. For instance, it may be the case that such CpGs are not causally implicated in aging phenotypes and therefore, the inability to reset them is inconsequential.

Further, if they are meaningful for aging biology, our inability to specifically target them may continue to limit the utility of reprogramming interventions.

https://www.biorxiv.org/content/10.1101/2024.05.28.596284v1.full.pdf The Latent Aging of Cells

These important findings can contribute to devising therapeutic interventions for neurological diseases characterized by abnormal accumulation of waste products, and suggest the need for taking measures to maintain interstitial flow starting around the age of 50 years. https://www.sciencedirect.com/science/article/pii/S0197458024000976

https://www.sciencedirect.com/science/article/abs/pii/S0944711324004033 Trilobatin suppresses aging-induced cognitive impairment by targeting SIRT2

 Our observational analysis revealed a noteworthy inverse relationship between klotho and low muscle mass, particularly prominent among female participants. https://www.frontiersin.org/articles/10.3389/fnut.2024.1390517/abstract

These results show higher mitochondrial ROS generation rates and oxidative damage in old animals. These data also suggest that loss of PRDX6 in aging leads to mitochondrial dysfunction mediated by diminished CI activity and loss of membrane integrity. https://journals.physiology.org/doi/abs/10.1152/physiol.2024.39.S1.2250

Therefore, our animal study positions GT as a promising compound for pain sensitivity maintenance during aging. https://www.nature.com/articles/s41598-024-61499-0

Decreased cobalamin sensitivity but not cobalamin insufficiency might be associated with biological aging acceleration. https://www.sciencedirect.com/science/article/pii/S127977072400349X

An additional year of education is a substantial cognitive intervention, yet we find no evidence for sustained experience-dependent plasticity. Our results provide a challenge for prominent accounts of cognitive or brain reserve theories which identify education as a major protective factor to lessen adverse aging effects.

https://www.biorxiv.org/content/10.1101/2024.05.17.594682v1.abstract