Rapamycin is Fantastic and Worth Trying

[Blossom]

I have been doing 20mg once a month lately.

That’s awesome. I might try a higher dose monthly at some point too. I heard in an interview recently with Matt Kaeberlin where he briefly talked about taking a high intermittent dose being the best chance at getting it past the BBB. I’m going to do a 5 week senolytic experiment first and depending on how that goes I might share those results here.

 

[Birdie]

.

 

[Birdie]

I find it's available through amazon pharmacy with a script.

 

[frannybananny]

.

May I ask where you are getting your Rapa? This is the cheapest that I have found it without a script and it is more than $2 a 1mg pill. Sirolimus 1 mg | buy repacan 1 mg Online | {20 % Off } |MedicineVilla Are you taking it yourself or just giving it to your husband? Appreciate any updates.

 

[Birdie]

May I ask where you are getting your Rapa? This is the cheapest that I have found it without a script and it is more than $2 a 1mg pill. Sirolimus 1 mg | buy repacan 1 mg Online | {20 % Off } |MedicineVilla Are you taking it yourself or just giving it to your husband? Appreciate any updates.

That's what I pay too, well $ 1.92 for the 1mg pill. I left a more detailed comment back where the dot is, but decided it was too personal. But, since you're interested !

I took 1mg two weeks ago, and 2mg this past week. Friday morning is my time. Good results.

Husband up to 3mg and intends to stay there for the time being. He's had great results. I'm in the midst of stuff now, but will report when I can. Rapa from ADC.

 

[frannybananny]

That's what I pay too, well $ 1.92 for the 1mg pill. I left a more detailed comment back where the dot is, but decided it was too personal. But, since you're interested !

I took 1mg two weeks ago, and 2mg this past week. Friday morning is my time. Good results.

Husband up to 3mg and intends to stay there for the time being. He's had great results. I'm in the midst of stuff now, but will report when I can. Rapa from ADC.

What do you mean "good results" and "great results"? Energy level?

 

[Birdie]

Thank you tarmander and blossom and everyone who posted about progress with Rapa. Here's my little report:

I started husband on a 1mg dose w breakfast on a Friday. The dose for the second week was 2mg. Dose for 3rd week was 3mg. Always Fridays at breakie.

Result wise, husband's hair texture and shine improvement was noticed by him week 3 using a 3mg dose. I'd noticed this improvement much sooner. And he reported previous occult (visible) blood in urine was no more at this time.

Toward the end of week 3 w the 3mg dose, he reported improvement in urine output and quality. Said he'd had foamy urine before starting Rapa but it was now clear. No more urgency noted. No nighttime up to pee.

Another improvement was that he no longer needed a nap, whereas he'd been needing one and sometimes two naps a day.

He wanted to and did keep the same 3mg dose for week 4. His motivation has hugely improved but I don't have time to add more here now.

 

[Blossom]

Thank you tarmander and blossom and everyone who posted about progress with Rapa. Here's my little report:

I started husband on a 1mg dose w breakfast on a Friday. The dose for the second week was 2mg. Dose for 3rd week was 3mg. Always Fridays at breakie.

Result wise, husband's hair texture and shine improvement was noticed by him week 3 using a 3mg dose. I'd noticed this improvement much sooner. And he reported previous occult (visible) blood in urine was no more at this time.

Toward the end of week 3 w the 3mg dose, he reported improvement in urine output and quality. Said he'd had foamy urine before starting Rapa but it was now clear. No more urgency noted. No nighttime up to pee.

Another improvement was that he no longer needed a nap, whereas he'd been needing one and sometimes two naps a day.

He wanted to and did keep the same 3mg dose for week 4. His motivation has hugely improved but I don't have time to add more here now.

Awesome @Birdie, thanks so much for sharing your experiences.

 

[frannybananny]

Thank you tarmander and blossom and everyone who posted about progress with Rapa. Here's my little report:

I started husband on a 1mg dose w breakfast on a Friday. The dose for the second week was 2mg. Dose for 3rd week was 3mg. Always Fridays at breakie.

Result wise, husband's hair texture and shine improvement was noticed by him week 3 using a 3mg dose. I'd noticed this improvement much sooner. And he reported previous occult (visible) blood in urine was no more at this time.

Toward the end of week 3 w the 3mg dose, he reported improvement in urine output and quality. Said he'd had foamy urine before starting Rapa but it was now clear. No more urgency noted. No nighttime up to pee.

Another improvement was that he no longer needed a nap, whereas he'd been needing one and sometimes two naps a day.

He wanted to and did keep the same 3mg dose for week 4. His motivation has hugely improved but I don't have time to add more here now.

Thank you for that @Birdie!! How about yourself....notice any difference in your skin, gums, etc?

 

[Birdie]

Awesome @Birdie, thanks so much for sharing your experiences.

You're very welcome. Thank you for your many updates Blossom.

 

[Birdie]

Thank you for that @Birdie!! How about yourself....notice any difference in your skin, gums, etc?

You're welcome franny. I'm newer into it so we'll see.

 

[ecstatichamster]

that’s super @Birdie and thank you for reporting!!

 

[Birdie]

A note:

Calorie restriction (CR) and intermittent fasting (IF) extend both the lifespan and healthspan in diverse species. However, CR is of little benefit when started in old age [73,173–178]. Fasting inhibits the mTOR pathway in young but not old mice [179,180]. By contrast, rapamycin strongly inhibits mTORC1 at any age.

Rapamycin for longevity: opinion article | Aging

Aging | doi:10.18632/aging.102355. Mikhail V. Blagosklonny

www.aging-us.com

 

[frannybananny]

A note:

Calorie restriction (CR) and intermittent fasting (IF) extend both the lifespan and healthspan in diverse species. However, CR is of little benefit when started in old age [73,173–178]. Fasting inhibits the mTOR pathway in young but not old mice [179,180]. By contrast, rapamycin strongly inhibits mTORC1 at any age.

Rapamycin for longevity: opinion article | Aging

Aging | doi:10.18632/aging.102355. Mikhail V. Blagosklonny

www.aging-us.com

@Birdie I thought you and others might be interested in this article about eye health. I've been having trouble with one of my eyes and am looking forward to receiving my rapamycin from IndiMart so I possibly might be able to halt any further deterioration of one of my eyes. >>
Age-related macular degeneration (AMD) is a leading cause of irreversible blindness among people of 50 year or older. During AMD, vascular endothelial growth factor (VEGF) may become elevated, causing choroidal neovascularization (CNV) and vascular permeability and fragility. Choroidal neovascularization can break in Bruch's membrane, resulting in subretinal hemorrhage, fluid exudation, detachment of the retinal pigment epithelium from the choroid, and formation of fibrotic scars [1]. Patients with neovascular age-related macular degeneration could suffer sudden visual loss due to subretinal hemorrhage or fluid accumulation secondary to choroidal neovascularization. Although neovascular AMD only accounts for less than 15% of the overall age-related macular degeneration, it is responsible for over 80 percent of the severe vision loss cases. Current therapeutics for neovascular AMD are two closely related antibody drugs, ranibizumab (trade name Lucentis) and bevacizumab (trade name Avastin), both of which bind to and neutralize VEGF [2,3]. Bevacizumab is a humanized anti-VEGF monoclonal antibody while ranibizumab is a humanized monoclonal antibody fragment that is made based on the same murine monoclonal antibody as bevacizumab. Ranibizumab is an FDA-approved drug but bevacizumab is used off-label by ophthalmologists. Both agents are used for intravitreal injections, which is cumbersome for patients and is not suitable for preventive treatment. Therefore, new drugs are needed to prevent and treat this type of disease.

It was reported in 2004 that rapamycin (trade name sirolimus) treatment significantly reduced the extent of neovascularization in both choroidal neovascularization and retinal neovascularization models induced in adult mice with laser photocoagulation and hyperoxia/hypoxia, respectively [4]. In an advance online publication this year in American Journal of Pathology [5], Kolosova et al presented exciting results that rapamycin could actually prevent AMD-like retinopathy in an aging rat model that more closely resembles human AMD pathology. They investigated the effect of rapamycin on spontaneous retinopathy in senescence- accelerated OXYS rats. OXYS rats were treated orally with either 0.1 or 0.5 mg/kg rapamycin, which was given together with food. Rapamycin was found in a dose-dependent manner to reduce the incidence and severity of retinopathy, and attenuated AMD disease progression. Some histological abnormalities associated with retinopathy were notably reduced. For examples, in retinal pigment epithelial cell layers, rapamycin decreased nuclei heterogeneity and normalized intervals between nuclei; in photoreceptor cells, rapamycin prevented nuclear and cellular pyknosis; significantly, rapamycin prevented destruction of ganglionar neurons in the retina. Rapamycin did not exert any adverse effects on the retina in control disease-free Wistar rats, suggesting that it is safe.

Rapamycin is a macrolide antibiotic and FDA-approved drug for organ transplantation, prevention of restenosis in cardiology and treatment of advanced renal cancer [6]. Chronic oral use of rapamycin is well tolerated in human patients, with mild side effects mainly being elevated triglycerides. These new results demonstrate a potential therapeutic utility of rapamycin for treatment and prevention of retinopathy in AMD and severe diabetes. Although rapamycin was previously reported to block VEGF expression [7], it did not significantly decrease VEGF levels in the murine AMD models [4,5], suggesting that rapamycin acts through a different mechanism. One possibility is that rapamycin inhibits VEGF stimulated intracellular signaling necessary for angiogenesis, which requires mTOR, the mechanistic target of rapamycin [8]. Evidence also accumulates that mTOR is a key aging factor. Genetic down-regulation of mTOR or rapamycin treatment in various model organisms ranging from the yeast S. cerevisiae, the worm C. elegans, the fruit fly D. melanogaster, and genetically heterogeneous mice, were found to significantly extend the lifespan of these organisms [6]. Moreover, rapamycin is known to reduce many age-related diseases such as AMD and Parkinson's disease [6]. Conceivably the AMD-preventive effect could be attributed to the overall anti-aging activity of rapamycin. Because diseases such as AMD are difficult to cure once they have developed, early chemoprevention is likely the best option. The findings that rapamycin prevents the progression of AMD in a more physiologically model provide a new hope for the high risk AMD population.<<

Chemoprevention of age-related macular regeneration (AMD) with rapamycin

www.ncbi.nlm.nih.gov

 

[frannybananny]

@Birdie I thought you and others might be interested in this article about eye health. I've been having trouble with one of my eyes and am looking forward to receiving my rapamycin from IndiMart so I possibly might be able to halt any further deterioration of one of my eyes. >>
Age-related macular degeneration (AMD) is a leading cause of irreversible blindness among people of 50 year or older. During AMD, vascular endothelial growth factor (VEGF) may become elevated, causing choroidal neovascularization (CNV) and vascular permeability and fragility. Choroidal neovascularization can break in Bruch's membrane, resulting in subretinal hemorrhage, fluid exudation, detachment of the retinal pigment epithelium from the choroid, and formation of fibrotic scars [1]. Patients with neovascular age-related macular degeneration could suffer sudden visual loss due to subretinal hemorrhage or fluid accumulation secondary to choroidal neovascularization. Although neovascular AMD only accounts for less than 15% of the overall age-related macular degeneration, it is responsible for over 80 percent of the severe vision loss cases. Current therapeutics for neovascular AMD are two closely related antibody drugs, ranibizumab (trade name Lucentis) and bevacizumab (trade name Avastin), both of which bind to and neutralize VEGF [2,3]. Bevacizumab is a humanized anti-VEGF monoclonal antibody while ranibizumab is a humanized monoclonal antibody fragment that is made based on the same murine monoclonal antibody as bevacizumab. Ranibizumab is an FDA-approved drug but bevacizumab is used off-label by ophthalmologists. Both agents are used for intravitreal injections, which is cumbersome for patients and is not suitable for preventive treatment. Therefore, new drugs are needed to prevent and treat this type of disease.

It was reported in 2004 that rapamycin (trade name sirolimus) treatment significantly reduced the extent of neovascularization in both choroidal neovascularization and retinal neovascularization models induced in adult mice with laser photocoagulation and hyperoxia/hypoxia, respectively [4]. In an advance online publication this year in American Journal of Pathology [5], Kolosova et al presented exciting results that rapamycin could actually prevent AMD-like retinopathy in an aging rat model that more closely resembles human AMD pathology. They investigated the effect of rapamycin on spontaneous retinopathy in senescence- accelerated OXYS rats. OXYS rats were treated orally with either 0.1 or 0.5 mg/kg rapamycin, which was given together with food. Rapamycin was found in a dose-dependent manner to reduce the incidence and severity of retinopathy, and attenuated AMD disease progression. Some histological abnormalities associated with retinopathy were notably reduced. For examples, in retinal pigment epithelial cell layers, rapamycin decreased nuclei heterogeneity and normalized intervals between nuclei; in photoreceptor cells, rapamycin prevented nuclear and cellular pyknosis; significantly, rapamycin prevented destruction of ganglionar neurons in the retina. Rapamycin did not exert any adverse effects on the retina in control disease-free Wistar rats, suggesting that it is safe.

Rapamycin is a macrolide antibiotic and FDA-approved drug for organ transplantation, prevention of restenosis in cardiology and treatment of advanced renal cancer [6]. Chronic oral use of rapamycin is well tolerated in human patients, with mild side effects mainly being elevated triglycerides. These new results demonstrate a potential therapeutic utility of rapamycin for treatment and prevention of retinopathy in AMD and severe diabetes. Although rapamycin was previously reported to block VEGF expression [7], it did not significantly decrease VEGF levels in the murine AMD models [4,5], suggesting that rapamycin acts through a different mechanism. One possibility is that rapamycin inhibits VEGF stimulated intracellular signaling necessary for angiogenesis, which requires mTOR, the mechanistic target of rapamycin [8]. Evidence also accumulates that mTOR is a key aging factor. Genetic down-regulation of mTOR or rapamycin treatment in various model organisms ranging from the yeast S. cerevisiae, the worm C. elegans, the fruit fly D. melanogaster, and genetically heterogeneous mice, were found to significantly extend the lifespan of these organisms [6]. Moreover, rapamycin is known to reduce many age-related diseases such as AMD and Parkinson's disease [6]. Conceivably the AMD-preventive effect could be attributed to the overall anti-aging activity of rapamycin. Because diseases such as AMD are difficult to cure once they have developed, early chemoprevention is likely the best option. The findings that rapamycin prevents the progression of AMD in a more physiologically model provide a new hope for the high risk AMD population.<<

Chemoprevention of age-related macular regeneration (AMD) with rapamycin

www.ncbi.nlm.nih.gov

There's also this newer study from 2022....

Rapamycin Improved Retinal Function and Morphology in a Mouse Model of Retinal Degeneration

The retina is an important visual organ, which is responsible for receiving light signals and transmitting them to the optic nerve center step by step. The retina contains a variety of cells, among which photoreceptor cells receive light signals and convert ...

www.ncbi.nlm.nih.gov

 

[Birdie]

@frannybananny thank you. I was told once that I had the beginnings of MD. Few years later told no evidence at all. I don't necessarily trust these opinions at all.

Nifty if Rapa helps anyway. I'm reading about Rapa for hours each day. Always more and am encouraged or fascinated.

 

[Birdie]

I just ran into this from Dr Green:


Hospitalized 11/5/23 - 11/18/23

Dear Friends,

I had a massive Upper GI bleed on Sunday, 11/5/23.

It started with Codfish. I thought a low carbohydrate diet would be good. I thought codfish was the perfect food; low calories, almost all protein, low fat. Was eating about a pound of codfish (boiled, no sauce) almost every day. Codfish is very high in purines. As a result of a very high purine diet from codfish, I developed gout.



After a month of a painful right wrist due to Gout, I decided to try a high dose Prednisone for a short period. Excellent response in 12 hours. Took prednisone for 3 days, 40 mg, 30 mg, 20 mg then stopped due to fluid weight gain. The problem was taking Eloquist. A blood thinner for atrial fibrillation and Ibuprofen for pain related to Gout. All 3 meds increase the risk of bleeding.



Sunday morning I had a massive upper GI bleed. In the hospital, I received excellent care when I was finally transferred to CICU, and treated by an excellent cardiologist who understood Cardiomyopathy. I have a very rare inherited cardiomyopathy (see My story, why I started on Rapamycin in 2016).

After 5 days of fluid overload which almost killed me. Then added a new drug for fluid overload which crashed my blood pressure (80/40) and caused shock liver with liver enzymes of 3000.

Minimal liver damage.



I figure the chance of survival of the UGI bleed with all the medical complications was about 25%. I attribute my survival to Rapamycin. Due to 8 years on Rapamycin I had no significant coronary artery disease. If I had coronary artery disease, I would have never tolerated all the stress and medical malpractice, and I would have coded.



Now home. Back to my usual state of health. No harm, no foul.

Rapamycin Treatment for Age Related Diseases

44-01 Westmoreland Street, Little Neck, New York 11363 Make a new appointment by emailing us at [email protected]

rapamycintherapy.com

 

[Birdie]

A trial in the Seattle area:

Rapamycin Trial

FDA approval clinical trial evaluating rapamycin in older adults with periodontal disease

www.rapamycintrial.com

 

[Sumbody]

I just ran into this from Dr Green:


Hospitalized 11/5/23 - 11/18/23

Dear Friends,

I had a massive Upper GI bleed on Sunday, 11/5/23.

It started with Codfish. I thought a low carbohydrate diet would be good. I thought codfish was the perfect food; low calories, almost all protein, low fat. Was eating about a pound of codfish (boiled, no sauce) almost every day. Codfish is very high in purines. As a result of a very high purine diet from codfish, I developed gout.



After a month of a painful right wrist due to Gout, I decided to try a high dose Prednisone for a short period. Excellent response in 12 hours. Took prednisone for 3 days, 40 mg, 30 mg, 20 mg then stopped due to fluid weight gain. The problem was taking Eloquist. A blood thinner for atrial fibrillation and Ibuprofen for pain related to Gout. All 3 meds increase the risk of bleeding.



Sunday morning I had a massive upper GI bleed. In the hospital, I received excellent care when I was finally transferred to CICU, and treated by an excellent cardiologist who understood Cardiomyopathy. I have a very rare inherited cardiomyopathy (see My story, why I started on Rapamycin in 2016).

After 5 days of fluid overload which almost killed me. Then added a new drug for fluid overload which crashed my blood pressure (80/40) and caused shock liver with liver enzymes of 3000.

Minimal liver damage.



I figure the chance of survival of the UGI bleed with all the medical complications was about 25%. I attribute my survival to Rapamycin. Due to 8 years on Rapamycin I had no significant coronary artery disease. If I had coronary artery disease, I would have never tolerated all the stress and medical malpractice, and I would have coded.



Now home. Back to my usual state of health. No harm, no foul.

Rapamycin Treatment for Age Related Diseases

44-01 Westmoreland Street, Little Neck, New York 11363 Make a new appointment by emailing us at [email protected]

rapamycintherapy.com

There is a connection with Rapamycin and gout. mTOR inhibitors seem to increase uric acid levels.

Not everyone develops gout with high uric acid, but low thyroid function seems to help those crystals form, causing gout in those circumstances. I remember reading a study referring to the fact a 1 degree drop in body temp was enough to cause the crystals to form when uric acid levels are elevated.

Alcohol is also an mTOR inhibitor and it is well known those who frequently develop gout should avoid alcohol. And those who use alcohol regularly, are also known to have higher incidence of gout vs. those who don't.

 

[Birdie]

I thought this might be useful to someone here:

"After experimentation, I have found that an antibiotic cream is more effective than isoconazole for getting rid of Rapamycin acne. Therefore these outbreaks are probably bacterial in nature and probably why they break out when you take Rapamycin. Makes sense to me".

Side Effects of Rapamycin (part 2)

Jerry we are seeing a lot bioavailability issues with rapamycin from compounding pharmacies… See here Bioavailability of Rapamycin From Compounding Pharmacy

www.rapamycin.news