Anti-Aging & weight-loss effects of Rapamycin

Very interesting compound that apparently is all the rage right now among the rich and youth-obsessed of silicon valley.

By age 72, I experienced angina and shortness of breath on small hills. As a trained pathologist I accepted the reality that I was in rather poor shape. My fasting blood sugar was up, my creatinine blood level was elevated indicating renal insufficiency and I couldn't fit into any of my pants.
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I decided rapamycin 6 mg once a week would be an aggressive treatment and 3 mg once every 10 days would be a conservative treatment. I decided to go with aggressive treatment.

January 2016, I began the rapamycin-based Koschei formula with intent to take it for one year; in what could euphemistically be called a “proof-of-concept” experiment.

I didn't have to wait one year; by 4 months the results were miraculous. I lost 20 pounds, my waist-line went from 38 inches to 33. I bought a pair of size 32 jeans and didn't have to wear joggers no more. I could walk 5 miles a day and ride a bike up hills without any hint of angina. Creatinine went from elevated to normal and fasting blood sugar went down.

I thought I was Lazarus back from the dead. It's now over 1 year and I feel great. I've also had no mouth sores, the most common clinical side-effect. For me, rapamycin is the world's greatest medicine.

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Some links:

chriskresser.com/the-keys-to-longevity-with-peter-attia/

roguehealthandfitness.com/rapamycin-anti-aging-medicine-an-interview-with-alan-s-green-m-d

And, supposedly, the only doc in the U.S. who will prescribe (but note that it's available at All Day Chemist, and perhaps elsewhere.)

rapamycintherapy.com

While it’s certainly an interesting compound, the problem with jumping to this without more data, at least based on my limited understanding, is that a confined eating window of 8 hours or so, a fat centric diet/metabolism, and a high-glycine diet may accomplish most or all of what rapamycin’s main method of action (preventing mTor from being chronically up-regulated) does. Suppversity has also had interesting discussion of this. Almost everyone who is into grass-roots anti-aging is already doing these things so it is not clear what adding a compound that does the same thing would do in an otherwise healthy person. Also, IMO, silicon valley types are bad role models for health because they assume that ultra-high-tech fixes are necessary without first addressing the fundamentals (like resolving chronically up-regulated insulin) and they trust “experts” who have been more sources of promoting poor health than fixes for it.

Also, episode 193 of the Tim Ferriss podcast is mostly about rapamycin and anti-aging. Recorded on Easter Island (Rapa Nui), where rapamycin was discovered.

tim.blog/2016/10/20/my-life-extension-pilgrimage-to-easter-island

From Ferriss' show notes:

This episode was a blast.It was a tropical exploration of biology, life extension, and all good things. This included a lot of Carménère wine and good old-fashioned ball busting.

I was joined by:

Peter Attia, MD (@peterattiamd), who rejoins the show (catch his last appearance here). He is a former ultra-endurance athlete (e.g., swimming 25-mile races), compulsive self-experimenter, and one of the most fascinating human beings I know. He is one of my go-to doctors for anything performance- or longevity-related. Peter earned his MD from Stanford University and holds a BSc in mechanical engineering and applied mathematics from Queen’s University in Kingston, Ontario. He did his residency in general surgery at the Johns Hopkins Hospital, and conducted research at the National Cancer Institute under Dr. Steven Rosenberg, where Peter focused on the role of regulatory T cells in cancer regression and other immune-based therapies for cancer.

David M. Sabatini, M.D., Ph.D. (@DMSabatini) of MIT’s Whitehead Institute for Biomedical Research. David is on a short list for the Nobel Prize for his work in elucidating the role of rapamycin and mTOR.

Navdeep S. Chandel, Ph.D., the David W. Cugell Professor of Medicine and Cell Biology at the Feinberg School of Medicine, Northwestern University. Nav established his lab there to further the understanding of how mitochondria work as signaling organelles to regulate physiology and pathology. He is also the author of Navigating Metabolism.

Perhaps you’ve heard of people in Silicon Valley taking metformin, rapamycin, and supplements for longevity. In this conversation, we dig into the real science, what current evidence supports (or doesn’t), and other important matters like how to staple properly, which fonts reasonable people use, and why Borat is a genius. Enjoy!

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Rapamycin alleviates inflammation and muscle weakness...in a rat model of myasthenia gravis

Rapamycin alleviates inflammation and muscle weakness...in a rat model of myasthenia gravis

CONCLUSIONS This study confirmed that a Treg/Th17 cell imbalance might be a cause of EAMG.

Furthermore, for the first time, we used an mTOR inhibitor, RAPA, to treat AChR antibody-positive EAMG rats. We observed symptom improvement in the EAMG animals after treatment, suggesting that the treatment was effective, which might be due to RAPA's ability to reverse the Treg/Th17 cell imbalance in EAMG.

Compared with those treated with CTX, RAPA-treated animals showed a low mortality rate and Lennon scores, but had improved body weights, indicating that RAPA is superior to CTX in treating EAMG to some extent.

Rapamycin Reduces Neurological Deficits after Transient Global Ischemia

Effects of mTOR on Neurological Deficits after Transient Global Ischemiahttps://www.ncbi.nlm.nih.gov/pubmed/28729914

Mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase and activation of its signal pathway plays an important role in regulating protein growth and synthesis as well as cell proliferation and survival.

In the present study, we examined the contribution of mTOR and its downstream products to brain injuries and neurological deficiencies after cardiac arrest (CA) induced-transient global ischemia.

CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. Our results showed that expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1) and p70 ribosomal S6 protein kinase 1 (S6K1) pathways were amplified in CA rats compared to their controls.

Blocking mTOR using rapamycin attenuated upregulation of pro-inflammatory cytokines (namely IL-1β, IL-6 and TNF-&#945, and Caspase-3, indicating cell apoptosis and also promoting the levels of vascular endothelial growth factor (VEGF) and its subtype receptor VEGFR-2 in the hippocampus. Moreover, the effects of rapamycin were linked to improvement of neurological deficits and increased brain water content observed in CA rats.

In conclusion, activation of mTOR signal is engaged in pathophysiological process during CA-induced transient global ischemia and blocking mTOR pathway plays a beneficial role in regulating injured neuronal tissues and neurological deficits via PIC, apoptotic Caspase-3 and VEGF mechanisms. Targeting one or more of these specific mTOR pathways and its downstream signaling molecules may present new opportunities for neural dysfunction and vulnerability related to transient global ischemia.

Positive effects of rapamycin in rat model of sports concussion

The post-therapeutic effect of rapamycin in mild traumatic brain injured rats ensuing in the upregulation of autophagy and mitophagy
https://www.ncbi.nlm.nih.gov/pubmed/28685977

Mild traumatic brain injury (mTBI), common in juveniles, has been reported to be caused by sports-related concussion. Many young children may suffer from post-concussion syndrome. mTBI, in early stages of life, could play a part in neuron apoptosis and degeneration, cognitive and motor coordination impairment, as well as dementia.

Our study was aimed at further investigating the post therapeutic efficacy of rapamycin in the recuperation of mTBI whiles at the same time investigating the metamorphosis in both autophagy and mitophagy in mTBI.

We created a weight-drop rat mTBI model with the administration of rapamycin at 4 hours after every mTBI. Behavioral tests of beam walking and open field task indicated the expected improvement of cognitive and motor coordination functions. Both western-blot and immunofluorescence examinations revealed increased Beclin-1 and PINK1 in the treated rats as well as reduction of Caspase-3 and cytochrome C. More so, the TUNEL staining evidenced curtailment of apoptotic cells following treatment with rapamycin.

The up-regulation of Beclin-1 and PINK1 and the down-regulation of Caspase-3 and cytochrome C extrapolate that rapamycin plays neuroprotective as well as anti-apoptotic role via interposition of both autophagy and mitophagy.

Rapamycin Lessens Periodontitis in Mouse Study

[h=2]Rapamycin treatment attenuates age-associated periodontitis in mice[/b]

double tap

SoCal Guy said:

Very interesting compound that apparently is all the rage right now among the rich and youth-obsessed of silicon valley.

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More so than the always odd silicon valley types, it's getting legit attention from anti aging researchers and anti aging scientists. I attended the conference that looks at the cutting edge of anti aging science/med and Rapamycin was a topic of interest which I posted here prior HERE. It's already being used clinically in dogs with much success apparently:

http://www.cnn.com/2016/10/06/health/rapamycin-dog-live-longer/index.html

Used incorrectly, it's very toxic stuff however.

The main thing with dosing, is for anti-aging, I recall you just take it once per week.

JPB said:

The main thing with dosing, is for anti-aging, I recall you just take it once per week.

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Yes supposed to be 2-5mg per week