#103

Cancer is ridiculously complex.

At first there’s an initiating factor. I don’t believe at all that rapamycin is a carcinogen.
Then you have growth of the cancer cells. This growth continues until the cancer cells sense overcrowding. I also don’t believe that a drug that slows cellular proliferation is contributing to cancer cell growth.
When they sense overcrowding, they then want out of Dodge, and they utilize a very complicated system of new vessel growth ( angiogenesis), and suppression of the host’s immune surveillance as well as a dependency on the pro inflammatory cytokines, IL6 and 8.
Now, does rapamycin play a role in promoting this metastatic stage . Well, it’s possible. This wouldn’t show up as causing a greater cancer incidence, but rather more aggressive disease. Is this the case? I don’t know, but I’m now concerned.

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#104

There’s a biochemist, Prof Thomas Seyfried at Boston College (https://www.bc.edu/bc-web/bcnews/science-tech-and-health/biology-and-genetics/targeting-cancer.html), who believes cancer has massive complexity, but much of it can be reduced to metabolic disorders. This may be why low/longevity doses of Rapamycin appear to dissuade cancer from taking hold: Rapamycin seems to improve metabolic health (at low doses). Seyfried has been researching very low carb combined with exogenous ketones and standard cancer treatments to “pause” tumor growth and metastasis. (I know low carb diets aren’t tremendously popular here). It’s one of the reasons I decided to personally try a low carb diet as a permanent lifestyle after my cancer. (I also was “lucky” in the type of cancer I had.). I’m far more healthy now than I was before I got the cancer (although I won’t credit keto/low carb for that — it was likely a series of four-day fasts combined with strenuous exercise — although keto probably allowed me to maintain it and not be starving/craving). Not sure if low carb/keto had anything to do with my cancer not coming back, and no real way to tell on an n=1.

It’s not the point of this thread, but I thought a secondary opinion on cancer as a metabolic health related disease (and relation to Rapamycin) is useful.

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#105

Without Metformin, Acarbose or other interventions, Rapamycin treatment would leads to worsened hyperglycemia and exacerbates glucose intolerance. How does it improve metabolic health?

What dose do you call low?

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#106

It depends what you mean by “metabolic health”. If you are talking about ATP/O efficiency at the cellular level then it probably does improve it.

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#107

I wish Dr. Blagosklonny’s all the strength and good luck. I’m deeply saddened by his diagnosis. His research in my opinion was ahead of his time. He’s the only anti-aging researcher who actually proposed a testable hypothesis for aging that was actually confirmed by experiments. A pioneer.

As for the responses to this thread, They’re filled (and i’m sorry to say) with pseudo-scientific gibberish (i even saw someone throw COVID vaccines into the mix).

The science of Rapamycin isn’t established by the anecdote of a person you happened to know. Many seem to have fallen into the anti-aging pursuit and let themselves either be misguided or deluded about the extent of the impact of these anti-aging drugs.

Rapamycin in mice, Even in very high doses (above human transplant) extended the median life by 23%. That’s the MEDIAN. Meaning half of them got even less than that. And it’s not hard to guess that the unlucky bottom 5-10% got marginal If any benefit at all. This is understandable given the somewhat sporadic nature of cancer development. And even those who had their life extended a decent amount, They still died of cancer eventually.
By the way, Most of those taking rapamycin for anti-aging (including Dr.Blagosklonny) are taking doses much lower than the mice. Many need a wake-up call if they think their 5mg-10mg a week will guarantee them a life free of cancer or a guaranteed life extension. This is coming from someone who is taking and will continue taking Rapamycin.

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#108

FWIW
Have posted this several times.

“Science” is NEVER established.

If you think “science” is established review
Stuart Firestein view. That I feel is correct.

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#109

Fortunately, I stocked up on ivermectin, a hose dewormer which may have additive effects when combined with a dog dewormer.

#110

So, 5-10 mg/week doesn’t guarantee cancer prevention. How much higher does it has to go in your opinion for cancer prevention then? Is there literature to show that much higher dose vs much lower dose is a better choice long term?

#111

I think the point here is Rapamycin doesn’t prevent cancer. Even all the ITP mice who lived longer on Rapamycin still died from cancer in the end. Just later.

However, Dr. B seems quite young to have this serious cancer. :frowning:

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#112

“ivermectin” was/is a medication for human use. It became a veterinary use afterwards.

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#113

This is true doesn’t prevent, just slows it, I remember some one in the aging field/cancer field… maybe Robert Weinberg? I could be wrong. He said “if you live long enough, you will eventually get cancer”. as eventually 1 of our cells will suffer a mutation due to the limitations on dna repair mechanisms. Seems to be the case with the mice in the ITP studies, seems rapamycin just slows it, doesn’t prevent it.

Last year 1 of my coworkers died at 31 due to blood cancer which isn’t age related at all at such a young age.

I don’t think we should assume rapamycin had anything to do with his cancer, we dont have enough info.

I’m curious if theres any long term data studies on kidney transplant patients that have been rapamycin for years? their cancer rates etc.

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#114

Yes but.
We don’t have a human prospective, double blinded , well powered study on intermittent dosing of healthy individuals determining if rapa prevents cancer. We have conflicting studies on renal transplant patients.
We have mice.
We have an anecdotal report on a human. But not just any human.

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#115

It’s natural to assume when there’s no enough information and this is what’s happening.

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#116

Risk of de novo cancers after transplantation: Results from a cohort of 7217 kidney transplant recipients, Italy 1997–2009

Our study findings confirmed, in Italy, the increased risks for cancer following Kidney Transplantation, and they also suggested a possible protective effect of mTORi [mTOR inhibitors] in reducing the frequency of post transplant cancers.

https://www.ejcancer.com/article/S0959-8049(12)00727-7/fulltext

There are such studies, but you have to keep in mind that most transplant patients lost their renal function because of prior serious health conditions (diabetes, lupus, etc.) and most of such patients receive cadaver kidneys with poor match. In other words, it’s not a healthy population to start with.

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#117

In the early tumorigenesis, autophagy, as a survival pathway and quality-control mechanism, prevents tumor initiation and suppresses cancer progression. Once the tumors progress to late stage and are established and subjected to the environmental stresses, autophagy, as a dynamic degradation and recycling system, contributes to the survival and growth of the established tumors and promotes aggressiveness of the cancers by facilitating metastasis.

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#118

A very interesting post and supports my suggestion that it’s possible for rapa to both prevent and promote cancer depending on the circumstances.
Much to consider.

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#119

“Use of mTOR inhibitors (mTORi) exerted, for all cancers combined, a 46% significantly reduced risk (95% CI: 0.4–0.7).”
Good enough for me.

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#120

Would be nice to know the circumstances.

#121

what made you decide on rapamycin and how long have you been on and dose? Thank you.

#122

So, assuming that autophagy in the beginning prevents cancer and once a cancer develops promotes cancer, how much autophagy should we be aiming for?

On contemplation, I think the answer is that we need some autophagy, but we don’t need to go overboard. Therefore a low-mid dose may be the best and we should forego a higher dose. Just my thinking out loud here.

1 Like