Search Results for: MTOR

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Hypothesis of mtor and AMPK in infants and children

Hypothesis of mtor and AMPK in infants and children

According to a study conducted in the 1980’s, babies have between 2 and 28 days of no growth, then a day of strong growth.
Maybe mtor suppression is useful even in young children and is suppressed during those 2 to 28 days at which point the body switches to anabolic and AMPK suppression.
Maybe children and adults aren’t so different in regards to the importance of cycling between expression and suppression of mtor and AMPK.

We will need to confirm that study and it’s data. We would also need a study that could track mtor and AMPK in babies as they go, daily or perhaps every 2 days as the smaple interval.

Autism spectrum disorder, mTOR and AMPK

Autism spectrum disorder, mTOR and AMPK

“Autism spectrum disorder (ASD) has a strong and complex genetic component with an estimate of more than 1000 genes implicated cataloged in SFARI (Simon0 s Foundation Autism Research Initiative) gene database. A significant part of both syndromic and idiopathic autism cases can be attributed to disorders caused by the mechanistic target of rapamycin (mTOR)-dependent translation deregulation. We conducted gene-set analyses and revealed that 606 out of 1053 genes (58%) included in the SFARI Gene database and 179 out of 281 genes (64%) included in the first three categories of the database (“high confidence”, “strong candidate”, and “suggestive evidence”) could be attributed to one of the four groups: 1. FMRP (fragile X mental retardation protein) target genes, 2. mTOR signaling network genes, 3. mTOR-modulated genes, 4. vitamin D3 sensitive genes. The additional gene network analysis revealed 43 new genes and 127 new interactions, so in the whole 222 out of 281 (79%) high scored genes from SFARI Gene database were connected with mTOR signaling activity and/or dependent on vitamin D3 availability directly or indirectly. We hypothesized that genetic and/or environment mTOR hyperactivation, including provocation by vitamin D deficiency, might be a common mechanism controlling the expressivity of most autism predisposition genes and even core symptoms of autism.”

Headline

https://www.mdpi.com/1422-0067/20/24/6332/pdf

Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus

Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus

Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus

“Persistent milk miRNA signaling adds a new perspective to the pathogenesis of T2DM and explains the protective role of breastfeeding but the diabetogenic effect of continued milk miRNA signaling by persistent consumption of pasteurized cow’s milk.”

http://link.springer.com/article/10.1186/s12986-019-0412-1?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Emodin-induced (HeShouWu) autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes. – PubMed – NCBI

Emodin-induced (HeShouWu) autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes. – PubMed – NCBI

Emodin significantly inhibited the viability of and induced apoptosis in L02 cells in a dose- and time-dependent manner. In addition, emodin increased the number of GFP-LC3 puncta in L02 cells and upregulated the expression of LC3B-II compared to those in control cells. Furthermore, emodin significantly decreased the expression of p-PI3K, p-AKT and p-mTOR in a dose-dependent manner compared to that in control cells without altering the expression of PI3K, AKT and mTOR. Notably, cotreatment with emodin and 3-methyladenine (3-MA) or rapamycin significantly increased and decreased the apoptosis rate of L02 cells, respectively, compared to that of cells treated with emodin alone.

Emodin-induced autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes. – PubMed – NCBI
Longevity, healthspan and aging: what you need to know

Longevity, healthspan and aging: what you need to know

As you age, it’s important to focus on maintaining your health and wellbeing. This means eating a healthy diet, getting regular exercise and ensuring you’re taking care of your mental health. But what about your physical health? What can you do to ensure you live a long, healthy life?

There are many things you can do to improve your lifespan and healthspan. Here are some of the most important:

  1. Eat a balanced diet

A balanced diet is key to good health. It’s important to include plenty of fresh fruits and vegetables in your diet, as well as whole grains, lean protein and healthy fats. Avoid processed foods and sugary drinks whenever possible.

  1. Get regular exercise

Exercise is essential for good health. It helps keep your body strong and healthy, and it can also help protect against diseases such as cancer. Aim for at least 30 minutes of exercise per day, five days per week.

  1. Take care of your mental health

Mental health is just as important as physical health. Taking care of your mental wellbeing can help protect against conditions such as anxiety and depression. Make sure you take some time for yourself each day to relax and de-stress. And if you’re experiencing any problems with your mental health, be sure to seek professional help.

  1. Stay hydrated

It’s important to stay hydrated by drinking plenty of water throughout the day. Dehydration can lead to a number of problems, including fatigue, headaches and dizziness. Drink at least eight glasses of water per day to stay hydrated.

  1. Get enough sleep

Getting enough sleep is essential for good health. Adults should aim for around eight hours of sleep each night. Poor sleep can lead to a number of problems, including fatigue, stress and anxiety.

  1. Take supplements if needed

In some cases, supplements may be necessary in order to maintain good health. Omega-3 fatty acids are a good example – many people don’t get enough omega-3s from their diet, so taking a supplement can be beneficial. Consult with your doctor before starting any new supplements, however – not all supplements are safe for everyone to take.

  1. Consider nmn therapy

nmN therapy is a novel treatment that uses neural modulation to improve cellular function and promote longevity [1]. The therapy involves injecting nmN into specific areas of the brain in order to promote cell rejuvenation [2]. so far, studies have shown that nmN therapy can improve cognitive function, increase lifespan and protect against age-related diseases [3].

8 . Consider rapamicin therapy

Rapamicin is a drug that has been shown to increase lifespan in animals [4]. It works by inhibiting the mTOR pathway, which is responsible for cell growth and aging [5]. Rapamicin has been shown to delay the onset of age-related diseases such as cancer and heart disease [6], and it may also be able to improve cognitive function [7].

9 . Consider metformin therapy

Metformin is a drug that is commonly used to treat diabetes [8]. However, research suggests that it may also have anti-aging properties [9]. One study found that metformin was able to extend the lifespan of worms by up to 50% [10]. Another study showed that metformin was able to reduce the risk of death from all causes in patients with type 2 diabetes [11] . While more research is needed on the anti-aging effects of metformin, it’s possible that this drug could play an important role in extending lifespan in humans .

Oncotarget | From rapalogs to anti-aging formula

Oncotarget | From rapalogs to anti-aging formula

Inhibitors of mTOR, including clinically available rapalogs such as rapamycin (Sirolimus) and Everolimus, are gerosuppressants, which suppress cellular senescence. Rapamycin slows aging and extends life span in a variety of species from worm to mammals. Rapalogs can prevent age-related diseases, including cancer, atherosclerosis, obesity, neurodegeneration and retinopathy and potentially rejuvenate stem cells, immunity and metabolism. Here, I further suggest how rapamycin can be combined with metformin, inhibitors of angiotensin II signaling (Losartan, Lisinopril), statins (simvastatin, atorvastatin), propranolol, aspirin and a PDE5 inhibitor. Rational combinations of these drugs with physical exercise and an anti-aging diet (Koschei formula) can maximize their anti-aging effects and decrease side effects.

http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=18033&path%5B%5D=57761

Eating to live…longer and healthier.

There are two main ways to provide the nutrients and the myriad of compounds that can help your body operate at its best and improve both lifespan and healthspan. One is to use supplements and the other is to do it via food in our diet.

Here, in the first of our three part series on direct action for longevity, we explore the foods you can incorporate into your diet to get those identified goodies that keep us healthy for longer. We will also include herbs here as food as they require little to no handling to be beneficial and can be consumed as a food. Some of this is known via human clinical trial while some may be a mix of anecdotal use or animal studies. In all cases we take a can’t hurt, might help, approach and will either call out or exclude anything showing any risk of harm.

It’s important to note that, while all care is taken, we cannot guarantee the accuracy of this information and you should consult your health care professional before making changes in your diet and lifestyle.

Continue reading “Eating to live…longer and healthier.”
Effects of dairy consumption on SIRT1 and mitochondrial biogenesis in adipocytes and muscle cells. – PubMed – NCBI

Effects of dairy consumption on SIRT1 and mitochondrial biogenesis in adipocytes and muscle cells. – PubMed – NCBI

“These data indicate that dairy consumption leads to systemic effects, which may promote mitochondrial biogenesis in key target tissues such as muscle and adipose tissue both by direct activation of SIRT1 as well as by SIRT1-independent pathways.”

Notice the word dairy is used, not milk. see our previous post on milkand its mTor activation and AMPK suppression.

https://www.ncbi.nlm.nih.gov/pubmed/22185590

DNA Testing

DNA Testing

Have you considered getting your DNA sequenced? Wonder what kind of information you could expect out of it?

I recently got my DNA sequenced at Self Decode and the results are in! Let’s take a look at whats in there and how I might be able to use it to improve my health and lifespan.

The introductory report shows me a high level overview of things I may want to dig deeper into.

Now, what does this mean and what can I do about it?

Typical risk of vit. k deficiency so, not much needed to be done here
Mostly typical ability to convert beta-carotene to Vit. A. Nothing to see here.
Seemingly normal ability to process B12. Good news.
I know I have one of two MTFHR gene mutations so no surprises here on Folate. I supplement with MTHF or Methyl-Folate to make up for this.
Now, I don’t drink Coffee, nor do I drink and caffeinated drinks so, nothing to worry about here. Basically I can process caffeine more readily.
Need to keep an eye on food intake. I have recently started intermittent fasting and have reduce my sugar and dairy intake (see our post about miRNA’s in milk expressing mTOR and suppressing AMPK).
Mix results here meaning no real action needed except that I should possibly target power training.
Typical Lipid levels. Not better or worse, just your regular ability to process lipids.
I never considered that DNA may influence something like my levels of empathy. I guess this explains why I’ve started Health Hacker to help people live healthier and longer lives.
Look out Black Friday and Cyber Monday, here comes an impulse shopper!
Anxiety is something I’ve struggled with for most of my life. I employ multiple strategies to help with it including CBD and B3, along with Omega-3.

Along with the report are sources to NIH publications to back the assertions. You also get deeper reports on each of those subject areas including MTFHR, APOE, Mood, Cognitive, Essential Minerals, Vitamins, Sleep, Cardiovascular, Inflammation and Fitness. You also get a personalised blog that shows you articles related to SNPs in your results.

I’m not saying that this is the best DNA service but it’s the one I chose and this is what I got. It seems quite comprehensive and does a good job at explaining what it all means and how I can adjust my diet and lifestyle to account for deficiencies caused by gene mutations. If this is something you are interested in then it might be an option for you.

Maf1‐dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan – Shetty – – Aging Cell – Wiley Online Library

Maf1‐dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan – Shetty – – Aging Cell – Wiley Online Library

Fundamental cellular mechanisms such as nutrient sensing, DNA damage response pathways, and cell cycle regulation influence the aging process. Studies have shown that the nutrient sensory kinase, mTOR (TOR in yeast), regulates lifespan in response to nutrient availability. The mTOR kinase forms two distinct protein complexes: TORC1 and TORC2. TORC1, which is inhibited by rapamycin, regulates cell growth, proliferation, and metabolism. It is well established that TORC1 promotes protein translation via phosphorylation of ribosomal protein S6 kinase and the eIF4E‐binding protein (BP; Zoncu, Efeyan, & Sabatini, 2011). The TORC2 branch is less studied; however, TORC2 also plays important roles in metabolism, cell survival, and proliferation (Zoncu et al., 2011). Although the involvement of the TORC1 pathway in lifespan regulation is conserved among many species (i.e., TORC1 inhibition extends lifespan), it is still unclear how this pathway affects multiple downstream stress and damage response mechanisms.

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13068?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

From Tea to treatment; Epigallocatechin Gallate and its potential involvement in minimizing the metabolic changes in Cancer

From Tea to treatment; Epigallocatechin Gallate and its potential involvement in minimizing the metabolic changes in Cancer

As the most abundant bioactive polyphenol in green tea, epigallocatechin gallate (EGCG) is a promising natural product that should be utilized in the discovery and development of potential drug leads. Due to its association with chemoprevention, EGCG may find a role in the development of therapeutics for prostate cancer. Natural products have long been employed as a scaffold for drug design, as their already noted bioactivity can help accelerate the development of novel treatments. Green tea and the EGCG contained within have become associated with chemoprevention, and both in vitro and in vivo studies have correlated EGCG to inhibiting cell growth and increasing the metabolic stress of cancer cells, possibly giving merit to its long utilized therapeutic use in traditional therapies. There is accumulating evidence to suggest that EGCG’s role as an inhibitor of the PI3K/Akt/mTOR signaling cascade, acting upon major axis points within cancer survival pathways. The purpose of this review is to examine the research conducted on tea along with EGCG in the areas of the treatment of and/or prevention of cancer. This review discusses Camellia sinensis, as well as the bioactive phytochemical compounds contained within. Clinical uses of tea are explored, and possible pathways for activity are discussed before examining the evidence for EGCG’s potential for acting on these processes. EGCG is identified as being a possible lead phytochemical for future drug design investigations.

https://www.sciencedirect.com/science/article/pii/S0271531719305007?dgcid=rss_sd_all&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Metformin

Metformin

Risks: this risk is low (less than 10 cases for 100,000 patient years), but the risk of metformin-induced lactic acidosis (MALA) increases in certain situations where both the plasma levels of metformin are increased and lactate clearance is impaired.[6] 

What is a stack and whats in one? – Opinion

What is a stack and whats in one? – Opinion

So you have a bunch of information on things that can help you live healthier and longer. What next?

Typically what a biohacker does is builds a stack. A stack is a collection of supplements that is aimed at a certain goal.

I’m going to give you some insight into my “pet rabbit” stack 😉 My rabbit is 104kgs and around 40 years old (Super Rabbit 😉 My rabbit is wanting to live healthier and longer as well as improve cognetive function and avoid cognitive decline. She wants to grow her hair and keep it a healthy colour and improve general health and fitness.

Firstly a dosing routine showing morning and evening dosing and which to take at what time of day for the desirable outcome.

Continue reading “What is a stack and whats in one? – Opinion”
3 Drug Combination Increases Lifespan | | LEAF

3 Drug Combination Increases Lifespan | | LEAF

We show that the mitogen-activated protein kinase kinase (MEK) inhibitor trametinib, the mTOR complex 1 (mTORC1) inhibitor rapamycin, and the glycogen synthase kinase-3 (GSK-3) inhibitor lithium act additively to increase longevity in Drosophila

https://www.leafscience.org/a-triple-drug-combination-increases-lifespan/

RAPAMYCIN Analogue found with minimal side effects

RAPAMYCIN Analogue found with minimal side effects

a study published by the University of Wisconsin in July, 2019, scientists discovered that a rapamycin analog called DL001 inhibits mTOR without all the severe side effects, such as suppression of the immune system, glucose, or liver toxicity. Suppression of mTOR has been associated with better health and longer life. mTOR is activated by eating foods like red meat, so finding a way to suppress mTOR without all the harmful side effects would be a major breakthrough.

Scientists have known that mTOR is composed of two complexes, called mTORC1 and mTORC2. As it turns out, you only need to suppress one of them, mTORC1 to get all the positive longevity benefits associated with rapamycin. Suppressing mTORC2 is what has caused many of the negative side effects of rapamycin, so discovering that the rapamycin analog DL001 suppresses mTORC1 without suppressing mTORC2 is the breakthrough that may finally allow us to get the benefits of rapamycin without the severe side effects.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642166/