Jay
#81
RapAdmin, This may have already been posted, but in case not, here is a publication from 2023 Oct 20 about the controversies of GDF-11. In particular, it notes that GDF-11 in humans does not decrease with age (though GDF-8 myostatin does) which I find very interesting. It doesn’t mean that adding more exogenous GDF-11 isn’t beneficial, but I wonder.
As an additional note, I have investigated GDF-11 several times the last few years and other than Steve Perry’s detailed account I find very few people here, on the forum.age-reversal.net or on Reddit who actually state that they’re using it. I even looked at the Facebook forum on GDF-11. When I asked those who were taking it about their results I got responses such as “I noticed nothing” to “I like the effects” but with no further details about the effects, and that was from less than a handful of responses I received. So, it just seems too nebulous to pursue. However, if you have tried it and can provide a precise account of your results that would be great.
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DrT
#82
There are recently published results that clearly show that GDF11 level in plasma of people aged 70+ is zero.
Earlier studies used inaccurate tests that could not distinguish between GDF11 and GDF8. Hence they showed no decline with age.
Many mouse study results should be treated with caution as they used gargantuan doses for the mice.
I have used GDF11 since about 2020, but I am not part of Steve Perry’s group.
I believe Steve has made available copious amounts of results from his participants.
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Jay
#83
DrT,
Thanks very much for the input. In the over 70 area I need all the help I can get. So, if you have time to tell more about your experience with GDF-11, especially any benefits, I would certainly like to hear it. Of course, any studies you can point to would be great, too.
Thanks,
Jay
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Please share details and results (if you have been able to measure any).
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Neo
#85
GDF11 improves hippocampal neurogenesis and cognitive abilities in diabetic mice by reducing neural inflammation
Highlights
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GDF11 treatment is shown to enhance hippocampal neurogenesis and ameliorate learning and memory deficits in a diabetic murine model.
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Targeted microglial depletion in diabetic mice via CSF1R inhibitor PLX5622 reduces neuroinflammation and improves cognitive function.
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The study delineates the neurogenic underpinnings critical for cognitive restoration, providing a potential therapeutic strategy for diabetes-associated cognitive decline.
https://www.sciencedirect.com/science/article/abs/pii/S0889159124004124
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Bicep
#86
So good to hear they didn’t forget about it. GDF11 has been such a mixed bag of conflicting results from different labs etc… Now it works in diabetic mice by reducing neural inflammation. Thanks Neo,
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More “mixed” results from GDF-11.
Primary GDF-11 proponent / user and biohacker Steve Perry died in August “after a brief illness”. Age 66 (he identifies as 64.5 years old in the 2022 video below).
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This is a shame. Young, and its people like Steve who move things forwards. Regardless of what caused it, it’s a lesson that all of this stuff has risks.
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Bicep
#89
Died suddenly? I’m thinking it had nothing to do with GDF 11.
I wish especially in this case that they would say what killed him. My obit will contain this information one way or another.
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Biology is really complex… I don’t think any post-mortem would ever be able to truly identify the cascade of biological changes that likely precipitated his death.
When a heavy user and leading proponent of an early-stage, experimental, non-FDA approved, and untested (in humans) therapeutic like GDF-11 dies an early death, I would say it increases my interest in waiting to see what the GDF11 clinical trials show…
There is a vast difference between taking an FDA-approved drug that has been in use for 20 years by hundreds of thousands of people around the world (like rapamycin), and injecting a relatively recently-identified chemical (GDF-11) that has little in the way of clinical data, and has gone through no formal clinical testing program, and is sourced from questionable suppliers off-shore…
https://www.nature.com/articles/s12276-020-00516-4
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Pat25
#91
This is really sad news. He had been so invested in GDF11 and the effects he felt it had on his health, and he seemed so full of enthusiasm about the future. Very sad to read this.
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hamtaro
#92
R.I.P. to Steve Perry. Although he was physically active, I think he admitted he did not follow a healthy diet, and didn’t have a healthy BMI. I think he stopped taking GDF11 for the last few years, but I could be wrong.
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I was impressed with Steve’s presentations on GDF-11. I really thought he presented a good case for it. I guess you really need those safety trials and RCTs before you start treatment on yourself. One more reason to be cautious with new treatments.
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Neo
#94
This I 100% agree with. And think he was taking other such compounds too?
For GDF11 I don’t think anyone has made a GMP / quality controlled / medical grade version available, rather all that has existed in the past has been different for research only products - not validated from a quality control perspective the way medicines have to be.
This piece I think needs a bit more nuance: Remember that GDF11 is found in our normal healthy blood and was originally found after analyzing parabiosis. It is natural and not a foreign chemical.
My understanding is that this natural protein is basically the same across all mammals. So in that sense we have hundreds of millions of years of “safety data” (whereas for many FDA approved molecules those are new and foreign to human - and even mammalian - biology).
Still I 100% agree that even natural human proteins or other blood products should be tested in clinical trials.
4 Likes
I’m in 
The titration should not be difficult. Someone posted that…
Found it GDF11 dilution calculation - Google Sheets
And another one…
Seems like there is more then 1 version of GDF11 available.
https://www.mybiosource.com/GDF11-peptide
Another source
https://www.miltenyibiotec.com/US-en/products/human-gdf-11.html#quality-grade=research-grade:size=20-ug
And another one
GDF11 levels fall to zero in humans at a mean age of 73.71. No endogenous GDF11 production results in the cessation of stem cell DNA repair which causes stem cells to die off and their populations fall to zero at an even faster rate. Since one cannot survive without hematopoietic, mesenchymal, etc. stems cells, this suggests that GDF11 may play a key role in maximum lifespan determination.
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I definitely don’t think the passing of Steve Perry is a good reason to discount either GDF11 or Klotho-both of which he used. I recall reading info from Steve Perry when I was seriously considering using Klotho. In the end, I concluded that the doses Steve Perry was advocating for, both for Klotho and GDF11, were much smaller than what would likely be needed to make a significant difference. See, for example, the dose he recommends in this GDF11 dilution spreadsheet (500 pg):
GDF11 dilution calculation - Google Sheets
Compared to the doses used in actual experiments and the total amount of GDF11 in the body (>1 mcg) that dose seems quite low. Here’s a list of doses from various experiments:
https://www.sciencedirect.com/science/article/pii/S0024320523002849
Notice how much higher those doses are (0.1 mg/kg and up being most common). Similarly, Klotho had an extremely low dose recommended
(over 1 million times smaller than in animal studies). This was the guide he made on Klotho dosing (0.5 pg/day):
Adding Klotho to your GDF11 Regimen - Google Docs
I am not very sure of GDF-11 either way, as I was only ever really intrigued by Klotho. In fact, I even randomly stumbled on a few negative articles on GDF-11 when looking up info about it:
In any case, I have a great deal of respect for Steve Perry as a pioneer in biohacking, and I don’t mean to be dismissive of his work. RIP Steve Perry.
4 Likes
DrT
#99
Such bad news.
I never met Steve face to face but we corresponded for some years about GDF11 (and cats.) He was generous with his time and his wisdom.
He freely admitted that his dietary habits were far from optimal and described himself to me as “King of the Late Night Pizza.”
I don’t know the cause of death. I really don’t know why next of kin withhold that information. It does no harm to know.
As much as I respected Steve’s cautious approach to GDF11 and his diligent gathering of evidence and information, I could never understand how such tiny doses could make a difference. I dose much higher.
But that’s just me.
One of Steve’s friends described him as a true “Renaissance Man” and I share that view.
Vale Steve
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One of my patients sent me this video that is a discussion from Elevian’s Physician.
I’m taking a different approach than Steve Perry on dosing now. This substance has about a 12 hour half life … so daily dosing to physiological levels makes sense. The approach of diluting down to homeopathic dosing levels seemed odd to me and completely counterintuitive. I cannot think of a scientific reason to do this. Can anyone?
I go for daily dose, but it is a challenge sorting out what a physiologic dose is, especially when there is no accessible test to monitor levels.
Same issue with Klotho - difficult and expensive to measure.
Hopefully some cost effective and accessible options will come forward in this space. The tests are available, with the klotho being $700 and the GDF-11 from a kit, but not anything one can order.
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Recombinant GDF11 Promotes Recovery in a Rat Permanent Ischemia Model of Subacute Stroke
Results: We confirmed rGDF11 activity in vitro and in established in vivo mouse models of cardiac hypertrophy and glucose metabolism and assessed the efficacy of rGDF11 treatment in six preclinical stroke studies, using independent Contract Research Organizations with all study animals and treatment groups blinded. All six studies revealed consistent improvement of sensorimotor outcomes with rGDF11. rGDF11-treated rats showed increased cortical vascularization and radial glia in the ventricular zone. Serum analysis revealed rGDF11 dose-dependent decreases in C-reactive protein and identified novel pharmacodynamic biomarkers and pathways associated with potential mechanisms of action of rGDF11.
Conclusion: These results demonstrate that systemically delivered rGDF11 enhances neovascularization, reduces inflammation, promotes neurogenesis, and improves sensorimotor function post-injury in a rat model of ischemic stroke. More importantly, these data define an optimized and clinically-feasible rGDF11 dosing regimen for therapeutic development in ischemic stroke and identify a panel of candidate pharmacodynamic and mechanistic biomarkers to support clinical translation.
https://www.ahajournals.org/doi/10.1161/STROKEAHA.124.049908
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