Tesamorelin vs. Ipamorelin?

[madhacker]

The IGF-1 Trade-Off: Performance vs. Longevity
Optimal IGF-1 Levels for Longevity

A meta-analysis analyzed ten studies on IGF-1 levels and all-cause mortality. The authors found a “U-shaped” association, meaning that IGF-1 levels on the low end and the high end of the spectrum were associated with increased risk of premature death.14​

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The lowest risk was at the 55th percentile of serum IGF-1, and increased in both directions for all-cause, cancer, and cardiovascular mortality.14 This data suggests that we should aim for an IGF-1 level near the lower to middle for healthy people in our age range.​

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Age: Average Serum IGF-1 (ng/ml)​

21-30 158-230​

31-40 135-220​

41-50 121-193​

51-60 98-150​

61-70 85-140​

71-80 85-95​

80+ 85-90​

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"Data on the IGF-1 system in relation to longevity are still controversial in long-lived subjects. One team described an increased plasma IGF-1/IGFBP-3 ratio in healthy centenarians compared to elderly subjects. They hypothesized that this elevated ratio was indicative of a higher IGF-1 bioavailability which contributed to the improved insulin action in centenarians. In contrast, others reported that subjects with at least an A allele of the IGF-1 receptor gene had low levels of free plasma IGF-1 and were more represented among long-lived people."

Insulin and IGF-1 in Human Aging and Longevity

 

[Cataceous]

"Data on the IGF-1 system in relation to longevity are still controversial in long-lived subjects. .... In contrast, others reported that subjects with at least an A allele of the IGF-1 receptor gene had low levels of free plasma IGF-1 and were more represented among long-lived people."
...

Growth Hormone Receptor Deficiency is Associated With a Major Reduction in Pro-aging Signaling, Cancer and Diabetes in Humans

...we monitored for 22 years Ecuadorian subjects with mutations in the growth hormone receptor gene leading to severe growth hormone receptor (GHR) and IGF-I deficiencies and combined this information with surveys to identify the cause and age of death for subjects who died before this period. The individuals with GHR deficiency (GHRD) exhibited only one non-lethal malignancy and no cases of diabetes, in contrast to 17% cancer and 5% diabetes prevalence in the controls. A possible explanation for the very low incidence of cancer may be revealed by in vitro studies: serum from GHRD subjects reduced DNA breaks but increased apoptosis in human mammary epithelial cells (HMECs) treated with hydrogen peroxide.​

...​

Here, we show that the fundamental link between pro-growth pathways, oxidative stress, age-dependent genomic instability and cellular damage observed in yeast (2, 15, 19-21), worms and mice (5, 6, 22-26) is conserved in humans by reporting on a 22-year monitoring of an Ecuadorian cohort with GHR and IGF-I deficiencies and by investigating the effect of these deficiencies on the cellular response to stress and on markers of cancer and diabetes.​

 

[madhacker]

LOL, you are a Valter D. Longo fan, now I understand your position. Valter doesn't believe in anything but supporting aging through lifestyle factors. I respect Valter, though the 2011 study you posted is one of four that are published by him supporting IGF and cancer risk and there are roughly 22 supporting cancer protective effects.

We could do this all day. I have provided an article that has sufficient new research supporting the benefits of restoring physiological levels of GH and IGF in aging people. Here's another one showing IGF-1 given late in life improving health span.

The reason I responded to your post is because I think it's irresponsible to give people advice, in absolutes. Your position as Valter's is only a hypothesis. There's a lot of new research supporting IGF's beneficial effects on health span. You can look up Nelson's posts on the subject as well.

Late-life targeting of the IGF-1 receptor improves healthspan and lifespan in female mice

 

[Cataceous]

LOL, you are a Valter D. Longo fan, now I understand your position. ...

Late-life targeting of the IGF-1 receptor improves healthspan and lifespan in female mice

Never heard of him. This was a reference cited by Curt Moyer in arguing against higher IGF-1 levels.

Your reference is pretty much saying the opposite of what you think it is. The monoclonal antibody treatment is for blocking the IGF-1 receptor. Basically if you turn off IGF-1 signaling then you get longer healthspan and lifespan in females.

The underlying mechanism(s) linking reduced IGF-1 signaling to improved mammalian lifespan is thought to involve improved stress defenses and lower risk for proliferative diseases9,10,11, though the reason for sex differences in this response remains unresolved.​

 

[madhacker]

Never heard of him. This was a reference cited by Curt Moyer in arguing against higher IGF-1 levels.

Your reference is pretty much saying the opposite of what you think it is. The monoclonal antibody treatment is for blocking the IGF-1 receptor. Basically if you turn off IGF-1 signaling then you get longer healthspan and lifespan in females.

The underlying mechanism(s) linking reduced IGF-1 signaling to improved mammalian lifespan is thought to involve improved stress defenses and lower risk for proliferative diseases9,10,11, though the reason for sex differences in this response remains unresolved.​

The research simply is not in support of your belief. A balance of mTOR and AMPK is important for healthspan and longevity.

Listen in at Rhonda Patrick at 5:45.

#02 - Rhonda Patrick, Ph.D.: the performance and longevity paradox of IGF-1, ketogenic diets and genetics, the health benefits of sauna, NAD+, and more - Peter Attia

 

[Cataceous]

The research simply is not in support of your belief. ...
...

And yet your own reference showed that the positive effects of lower IGF-1 are widely accepted. The first words of the abstract:

Diminished growth factor signaling improves longevity in laboratory models, while a reduction in the somatotropic axis is favorably linked to human aging and longevity. Given the conserved role of this pathway on lifespan, therapeutic strategies, such as insulin-like growth factor-1 receptor (IGF-1R) monoclonal antibodies (mAb), represent a promising translational tool to target human aging.​

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Sorry, not going to wade through a video. Quote some published studies.

In general summary articles what's being argued is that while higher IGF-1 does cause problems, maybe we can work around that by providing artificial stressors via diet to mimic the effects of lower IGF-1.

 

[madhacker]

And yet your own reference showed that the positive effects of lower IGF-1 are widely accepted. The first words of the abstract:

Diminished growth factor signaling improves longevity in laboratory models, while a reduction in the somatotropic axis is favorably linked to human aging and longevity. Given the conserved role of this pathway on lifespan, therapeutic strategies, such as insulin-like growth factor-1 receptor (IGF-1R) monoclonal antibodies (mAb), represent a promising translational tool to target human aging.​

​

Sorry, not going to wade through a video. Quote some published studies.

In general summary articles what's being argued is that while higher IGF-1 does cause problems, maybe we can work around that by providing artificial stressors via diet to mimic the effects of lower IGF-1.

Cataceous,

I first gave you an article that cited numerous studies and you have not done your homework. It's clear you do not have a background in bioscience as you do not know how to debate. I added that video because you are at the level of which it would be beneficial for you to hear from a leading scientist.

This is silly, I'm out. Do your homework, you don't have an idea of what you are talking about.

 

[Cataceous]

... Do your homework, you don't have an idea of what you are talking about.

Says the guy whose reference contradicts his viewpoint.

Even the cheerleading article in the Lifespan Journal acknowledges:

A not negligible number of studies have shown a positive association between higher serum IGF-1 levels and increased risk of breast cancer...​

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Some evidence points to the possibility that colon cancer might be favored by increased IGF-1 levels...​

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This piece uses the problems seen with low levels to argue in favor of high levels. But they conveniently overlook the unfavorable mortality studies and the lack of diabetes and cancer in those with Laron syndrome.

Dr. Longo said he believed that having very low levels of IGF-1 was the critical feature of the Laron patients’ freedom from age-related diseases. In collaboration with Dr. Guevara-Aguirre, he exposed human cells growing in a laboratory dish to serum from the Laron patients. The cells were then damaged with a chemical that disrupts their DNA. The Laron serum had two significant effects, the two physicians reported on Wednesday in Science Translational Medicine.​

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First, the serum protected the cells from genetic damage. Second, it spurred the cells that were damaged to destroy themselves, a mechanism the body uses to prevent damaged cells from becoming cancerous. Both these effects were reversed when small amounts of IGF-1 were added to the serum.​

 

[madhacker]

Says the guy whose reference contradicts his viewpoint.

Even the cheerleading article in the Lifespan Journal acknowledges:

A not negligible number of studies have shown a positive association between higher serum IGF-1 levels and increased risk of breast cancer...​

​

Some evidence points to the possibility that colon cancer might be favored by increased IGF-1 levels...​

​

This piece uses the problems seen with low levels to argue in favor of high levels. But they conveniently overlook the unfavorable mortality studies and the lack of diabetes and cancer in those with Laron syndrome.

Dr. Longo said he believed that having very low levels of IGF-1 was the critical feature of the Laron patients’ freedom from age-related diseases. In collaboration with Dr. Guevara-Aguirre, he exposed human cells growing in a laboratory dish to serum from the Laron patients. The cells were then damaged with a chemical that disrupts their DNA. The Laron serum had two significant effects, the two physicians reported on Wednesday in Science Translational Medicine.​

​

First, the serum protected the cells from genetic damage. Second, it spurred the cells that were damaged to destroy themselves, a mechanism the body uses to prevent damaged cells from becoming cancerous. Both these effects were reversed when small amounts of IGF-1 were added to the serum.​

You got it all figured out. You aren't educated so you can't read the literature to have a deep understanding. Good luck!