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  LongeCity
              Advocacy & Research for Unlimited Lifespans

Health View Source: Health Last Updated: 25 December 2024 - 12:07 PM

A group buy for TAC and other anti-aging medications. 23 December 2024 - 08:00 AM

We are organizing a group buy for TAC. With a larger quantity, we can definitely get a better price. If you're interested, Please let us know the quantity so we can tally up the total..We guarantee the authenticity and high quality of the products. All of these products can be sent for third-party testing to verify their content. If you have any other anti-aging products for which you cannot find a high-quality and reasonably priced source, feel free to let us know. China has everything you need. What sets us apart is our guarantee of quality.

 

TAC is a TERT activator compound that delays aging through two pathways: by extending telomeres and regulating gene expression.

 

Hong Seok Shim et al., TERT activation targets DNA methylation and multiple aging hallmarks.

Cell Doi: https://doi.org/10.1...ell.2024.05.048

 

In preclinical experiments, researchers treated elderly mice (equivalent to humans over 75 years old) with TAC for 6 months. The results showed that these older mice exhibited many "youthful" characteristics, such as enhanced cognitive abilities, the generation of new neurons in the hippocampus of the brain, and an increase in certain genes related to learning, memory, and synaptic biology. Additionally, neuromuscular control was strengthened, muscle strength and coordination improved, and the common issue of sarcopenia in older animals was reversed.

 

Tests on samples like blood and brain tissue also revealed that the elderly mice treated with TAC significantly reduced inflammatory responses, with a decrease in various disease-related inflammatory cytokines. They also eliminated accumulated senescent cells by inhibiting the key aging factor, the p16 gene.

 

At the same time, safety tests indicated no significant toxicity, including cancer risk.

Sleep hacks for counteracting Nicotine's negative effect on sleep? 21 December 2024 - 05:27 PM

I get A LOT out of Nicotine:

  • it's given me the stress relief I needed to get through a few challenging personal life things this year.
  • it consistently clarifies my thoughts and pushes me in a positive direction, personally and professionally.
  • it's better for my HRV than any other Nootropic I've tried.
  • It seems to be good for my immune system: The only times I've got ill in the past almost 10 years were the two very easy cases of COVID-19, which I powered right through on Nicotine.
  • And nothing unleashes my creativity (which my work and career depend on) more than Nicotine. I'm about 2/3 of the way through my first science fiction novel, thanks to NIcotine!
But, it's coming at an increasingly steep cost in my sleep quality: my issue is not sleep latency, I always fall asleep quickly, but early morning wake-ups.

Like, last night, I did 10mg of melatonin and woke up for some stupid reason at 3:30AM. Did I think 10mg melatonin more, fell back asleep, woke up and 6:30 AM, tossed and turned

Lots of nights are like last night. This is bad, I know.

I'm doing a lot of sleep hacks: blue blockers, no bright screens before bed, red light therapy, mouth taping, but my body just demands I get up at the asscrack of my dawn.

 

Please spare me the obvious advice of: QUIT NICOTINE DUDE - I'll do that when I finish writing my novel. What I'm looking for is something that might offset Nicotine's effect, a sleep supplement that will keep me asleep.

I'm married, and sometimes in marriage, you don't get what you want. My wife refuses to go to bed before midnight, so I'm running on 6 hours of sleep a lot of days.

 

I take Nicotine daily, but I'm not a voracious consumer: I take a maximum of 3 small .25ml hits of 10% USP solution and a few 2mg lozenges daily. That's how I often start the day.

 

Leave me some suggestions of more potent sleep hacks (I think I'm already doing all the mainstream ones) or some pharmacological suggestions for offsetting Nicotine's effect on sleep duration. Something to do with GABA I'm thinking...

 

I'm hoping I don't have to choose between finishing my novel and getting the sleep I need, because, to quote Eddie from the Limitless movie: "What's my excuse for looking like this? I'm a writer!"

is Brighton Laboratory a good lab to test supplements? 16 December 2024 - 04:19 AM

Prohealth is using them for their COA.  Is this a real lab?  I can't find anything online other than their website.  They used to use another lab I had heard of.

 

The new COA looks very Excel.

Your immune cells are what they eat 13 December 2024 - 06:17 PM

So, how would one correct this imbalance?

 

https://www.salk.edu/news-release/your-immune-cells-are-what-they-eat/

 

LA JOLLA—The decision between scrambled eggs or an apple for breakfast probably won’t make or break your day. However, for your cells, a decision between similar microscopic nutrients could determine their entire identity. If and how nutrient preference impacts cell identity has been a longstanding mystery for scientists—until a team of Salk Institute immunologists revealed a novel framework for the complicated relationship between nutrition and cell identity.

The answers came while the researchers were exploring different kinds of immune cells. The immune system relies on specialized “effector” T cells to fight off pathogens, but in chronic infections like HIV or cancers, the perpetual activation of these cells can turn them into “exhausted” T cells unable to continue fighting. In the new study, Salk scientists discovered that a nutritional switch from acetate to citrate plays a key role in determining T cell fates, shifting them from active effector cells to exhausted cells. This finding highlights how metabolic changes influence T cell identity and opens avenues for interventions to sustain immune function.

The discovery that different nutrients can change a cell’s gene expression, function, and identity significantly advances scientists’ understanding of the relationship between nutrition and cellular health throughout the body. It may also be possible to develop new therapies that target these nutrient-dependent mechanisms to help T cells stay active and energetically optimized against chronic diseases like cancer or HIV.

The findings were published in Science on December 12, 2024.

“You know the saying, ‘You are what you eat?’ Well, we uncovered a way in which this actually operates in cells,” says Professor Susan Kaech, senior author of the study and holder of the NOMIS Chair at Salk. “This is really exciting on two levels: on a fundamental level, our findings show that a cell’s function can be directly linked to its nutrition; on a more specific level, this sheds new light on how T cells become dysfunctional or exhausted and what we could do to prevent that.”

Glucosamine Causes Muscle Atrophy in Mice 06 December 2024 - 03:18 PM

Glucosamine inhibits myoblast proliferation and differentiation, and stimulates myotube atrophy through distinct signal pathways

J Nutr Biochem. 2025 Jan:135:109762. doi: 10.1016/j.jnutbio.2024.109762. Epub 2024 Sep 7.
Shui-Yu Liu  , Luen-Kui Chen, Yi-Ting Chung, Chien-Wei Chen, Guan-Lin Wu, et al.
Glucosamine (GlcN) is one of the dietary supplements used in the treatment of osteoarthritis. Endogenously, GlcN is synthesized from glucose through the hexosamine pathway. In addition to ameliorating arthritis, several biological functions of GlcN have been reported, including insulin resistance in skeletal muscle. However, the regulatory role of GlcN in skeletal muscle development is not clear. We therefore investigated the effect of GlcN on myoblast proliferation, differentiation, and myotube development and their underlying mechanisms in C2C12 cells. Myoblast proliferation was measured by MTT assay. The expressions of MyoD, myogenin (MyoG), and myosin heavy chain (MyHC) were identified as determinants of myoblast differentiation. Expressions of atrogin-1 and muscle RING-finger protein-1 (MuRF-1) were identified as markers of myotube atrophy. The results show that treatment with GlcN significantly reduced myoblast proliferation and phosphorylation of Stat3 and S6K. These findings suggest that GlcN can inhibit growth of myoblasts through inhibiting phosphorylation of Stat3 and S6K. In addition, GlcN significantly suppressed the expression of MyoD, MyoG, and MyHC, as well as myotube formation. Pretreatment of C2C12 myoblast cells with ER stress inhibitors significantly blocked GlcN-inhibited MyHC expression and myotube formation. It can be concluded that GlcN suppressed myogenic differentiation via a pathway that involved ER stress. Moreover, GlcN decreased myotube diameter and expression of MyHC, as well as increased MuRF-1 in C2C12 myotubes. Meanwhile, GlcN also reduced the expressions of phosphorylated Akt and mTOR were stimulated after GlcN treatment in C2C12 myotubes. Thus, GlcN induced skeletal muscle atrophy by inhibiting the protein synthesis pathway. Chronic GlcN infusion also caused skeletal muscle atrophy in mice. In conclusion, GlcN regulated important stages of skeletal muscle development through different signaling pathways.
PMID 39251145

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