My wife used 8mg rapamycin a week for 12 weeks and off 4 weeks . Does everything but taurine . What is your Rapamycin schedule and dose?

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So if I understand you are doing the rapamycin and this taurine every day. I too am dealing with bone loss and started taking this Rapamycin to stop the loss. I would love to know how much are you taking of both? I am reading about 6 grams on the taurine? I am currently taking Rapacan 2 mg every week and slowly moving up my dosage. I have had to take breaks to give my body time off since it has had a harder time with side effects but fell I am in a good spot now.

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Yes… as a 185 pound 6ft tall toned body male… I take 6 mg rapamycin/zydus once a week.

I take about 6 grams… one full teaspoon of taurine in my coffee… every morning with a teaspoon of creatine.

At night I take K2 vitamin and a calcium supplement.

No doubt this reversed my DEXA bone density score in one year from osteopenia -1.2 to normal at -.8


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I believe that low bone density is not necessarily the main cause of increased fracture rate. Poor balance and brittle bone is probably a bigger factor.

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I’ve been taking Taurine subcutaneously - haven’t taken any specific tests to show the impact but based on all of the positive studies, I will keep taking it.

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Reminded me of this MR preprint:

Moreover, mTOR inhibition significantly reduced body mass index (BMI), basal metabolic rate (BMR), height, and age at menopause, while increasing bone mineral density.

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So far as I can tell, the basic cause of osteoporosis is that osteoblasts don’t do their job well. This may be a general problem with stem cells losing function.

Rapa (sayth google) can affect osteoblasts. Hopefully, the effect is more positive than not …

Rapamycin, a small molecular inhibitor of the mammalian target of rapamycin (mTOR), can affect osteoblasts in a number of ways, including:

  • Preserving osteoblast viability: Rapamycin can reduce apoptosis and preserve osteoblast viability in the presence of lipotoxic concentrations of palmitate ¶.
  • Inducing osteoblastic differentiation: Rapamycin can induce osteoblastic differentiation in human embryonic stem cells (hESCs) by stimulating the BMP/Smad pathway.
  • Promoting autophagy: Rapamycin can induce autophagy, which can protect osteoblasts.
  • Inhibiting osteoblast proliferation and differentiation: Rapamycin can inhibit osteoblast proliferation and differentiation in MC3T3-E1 preosteoblastic cells and primary mouse bone marrow stromal cells.
  • Impairing bone accrual: Rapamycin can impair bone accrual in young adult mice.

https://www.google.com/search?q=osteoblast+rapamycin&sca_esv=ecab62f8c07129e5&rlz=1C5CHFA_enUS830US830&sxsrf=ADLYWIKrnuQiM4IuLMG7NoreocJMJxWA1Q%3A1736101117702&ei=_cx6Z9bHKpLP0PEP_O-k2QY&ved=0ahUKEwiWuqjTmN-KAxWSJzQIHfw3KWsQ4dUDCBA&uact=5&oq=osteoblast+rapamycin&gs_lp=Egxnd3Mtd2l6LXNlcnAiFG9zdGVvYmxhc3QgcmFwYW15Y2luMggQIRigARjDBDIIECEYoAEYwwQyCBAhGKABGMMEMggQIRigARjDBEitGlAAWMYRcAB4AJABAJgBUKAB4wSqAQIxMLgBA8gBAPgBAZgCCqAC-ATCAgYQABgHGB7CAgcQABiABBgNwgIIEAAYBxgIGB7CAgsQABiABBiGAxiKBcICChAhGKABGMMEGAqYAwCSBwIxMKAH9DM&sclient=gws-wiz-serp

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Beth my score at 60 was spine -2.5 and the other 2 places -1.9. I had not had a DEXA until I broke femur 7 years later and was so pleased that it was the same. Still not good but expected much worse due to my fatigue/lack of exercise. I think it had to be the HRT that kept it stable. Have one scheduled for May which will be another 4 years. I do take calcium, K, D, creatine, and recently added a collagen powder that algae cal makes. I will now add taurine, but think HRT has worked the best for me. If only I’d started it at 50 but nobody told me I should and even now a lot of docs don’t like it.

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Yep, what I read says that HRT is good, up to about age 60. I gather they think it shouldn’t be started after 60, but is ok to continue if it has been started, depending on the person.

It helps, but I’m still hoping for an actual cure, that is, kickstarting the osteoblasts into action again, something that will work at any age & gender.

FWIW, vida útil.io is featuring an article on helping out MSC’s, so far in mice, but they thing they have results to explore more: Keeping Stem Cells Healthy and Young | Lifespan.io

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Hi Elizabeth I’ve heard that re if you haven’t taken before 60, or 10 years after menopause, but it’s controversial. Some docs now say can take anytime. I have a friend just started pellets at 79 and is feeling great much better sleep more energy etc. I feel the same on or off just take for bones. At 60 was given estrone which I’ve recently read won’t help bones as it’s such a weak estrogen but it had to be what helped mine. I asked to have a level drawn after 7 years and the doc didn’t think necessary as “it’s a standard dose.” It was actually a lesser dose than that. I persisted and estrogen was 557! There again some docs said ok one NP said get off immediately. So many opinions out there. I’m now on an estradiol patch but it has no testosterone. Another thing I take forgot to mention is stronium so maybe it’s been helping too.

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Wait, mTOR inhibition makes women hit menopause earlier in life? That doesn’t make any sense. What am I missing?

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That has to be a typo, an unfortunate one.

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Are the gains maintained after discontinuing?

Yes, esp. if you “seal” the bone with short-term use of bisphosphonates. The gains will remain for decades.

Do you have any sources that support this idea? I’ve never heard of anything like this.

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Nope, not a typo, but they accept it is a counterintuitive finding, I’d weigh any RCT more than the MR though:

One counterintuitive MR result obtained by us is a reduction in age at menopause caused by
genetically-proxied mTOR inhibition. Rapamycin is currently being evaluated for a
favourable effect on reproductive aging in humans in the VIBRANT trial (ClinicalTrials.Gov
NCT05836025) since it was found to increase ovarian lifespan in mice previously92,93.
Furthermore, in a prospective cohort study, women with early onset of menopause had a
shorter life expectancy (-3.3 years) relative to healthy women experiencing menopause at a
normal age94

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I am an MD if that helps. Worked with an osteologist before and I asked him what he would do if he himself had osteoporosis. His response: 1) Take teriparatide for 2 years. 2) Do a single infusion of zoledronic acid (or oral olendronate for a couple of months) to prevent some bone loss (as after teriparatide the bone is in a state of increased remodeling resulting in rapid loss upon cessation of teriparatide - bisphosphonates prevent this state of heightened remodelling/bone loss).

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Congrats on the results! My bet it that it’s the vitamin K2 that caused it. I have never seen any indications or evidence of taurine being able to improve bone density and can’t think of a mechanisms by which it would be able to do so. In contrast, there is evidence of K2 increasing bone density.

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Hello Olafur -

My research and results say different.
Granted it’s rats… Effects of taurine supplementation on bone mineral density in ovariectomized rats fed calcium deficient diet - PMC

Yes, according to research, taurine can potentially improve bone density by stimulating bone formation and inhibiting bone resorption, suggesting it could be beneficial for maintaining bone health, particularly in conditions like osteoporosis; however, more research is needed to fully understand its mechanisms and optimal dosage for bone health.

Key points about taurine and bone density:

  • Osteoblast activity:

Taurine promotes the activity of osteoblasts, the cells responsible for building new bone tissue.

  • Reduced bone resorption:

Studies indicate taurine may help inhibit the activity of osteoclasts, cells that break down bone tissue.

  • Mechanism of action:

Taurine is thought to influence bone metabolism by impacting the differentiation and function of osteoblasts through various signaling pathways.

  • Potential benefits:

Taurine supplementation may be beneficial for individuals at risk of osteoporosis or experiencing bone loss.

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It may theoretically have potential to increase BMD, but in this study you linked to, taurine did not increase BDM at all. From the results section:

“In the control diet, spine BMD was significantly lower in OVX rats than in SHAM rats (0.095 ± 0.01 and 0.084 ± 0.08 g/cm2, respectively p<0.05), and in the taurine group, spine BMD was significantly lower in OVX rats than in SHAM rats. They were not significantly different from each other within SHAM and OVX groups by taurine supplementation (Table 7).”

“Mean femur BMD and BMC in the taurine diet group did not differ significantly from that in the control diet group in OVX rats fed 50% of recommended Ca diet. Also femur BMD/weight and BMC/weight of taurine group was not significantly higher than that of control group in OVX rats. (Table 8).”

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