GDF11, Elevian News Story - NYTimes

Wyss-Coray, a pioneer in parabiosis also has a similar type patent (earlier filing date). First half is a product patent.

The Conboys, also pioneers in this space also have patent applications:


I don’t care about epigenetic aging…I only care about translation (“did it make the rats demonstrably younger in actuality”), and that’s your 2nd question. It might be a setback, especially if other labs fail to show efficacy and repeatability. And to think this was likely rat-rat, never mind pig-human, which would be a natural global scale commercial model.

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Agreed, but you wouldn’t believe the exuberance and hype when E5 significantly impacted epigenetic aging. The hype train took off before any actual longevity studies were performed.

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The so-so study, which still has some treated rats alive after all the controls have died, was all female. The earlier, hyped study was all males. Their new study is half and half. They’re also doing something with Johns Hopkins, not sure what that study is.

You never responded to my query on your thoughts about the safety/efficacy of using animals as donors for human recipients?

Here’s an interesting history using animal donors for humans:

Genetically modified pigs seems to be our best bet.

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Xenotransplantation is progressing well

Amazing…who knew the rich history of xenotransplantation, and how very close we are to engineering pigs with very low transplant rejection, including plasma factors.

“Jean Baptiste Denis (1650) began the clinical practice of blood transfusion from animals to humans”

You are right…I think Josh Mittledorf (evolutionary aging theorist) bet his reputation on it.

Some background on young/old blood:

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Given the hyperbole and huckerism around GDF11, I’ll put this in the “probably not, but keep an open mind” category. The last straw for me was when I saw the study’s “suggested donation” of $15,000. I’ll wait for further, unbiased science.

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I agree - I’m watching from the sidelines on this one, and wish that Steve Perry partnered with an academic lab to validate his results and bloodwork / biomarker results. He quotes results from certain patients… Patient 15, 22, 24, etc… what about the other patients? seems to be cherry picking the data…

I do find his commentary on the Emfit interesting: Emfit QS+Active, sleep tracker and monitor with heart-rate-variability | Emfit web-shop USA, Mexico & Canada

A recent presentation on his results:

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Most of aging is caused by the atrophy of our stem cell population.

This seems like pure speculation. It may be an important cause, but it might not be a limiting cause of aging.

Why does the research consider these the Big Four biomarkers: BP, pulse, HRV, and reaction time?

on GDF11: “there is no other way on the planet to reduce reaction time.”

I don’t know how they measure reaction time or whether Steve Perry practices improving his reaction time, but I know that for specific tasks, reaction time can be improved with practice.

It strikes me that most all of these improvements are similar to the improvement due to exercise and weight loss. Since these patients apparently knew they were getting GDF11 injected, they might have changed their lifestyle as a result of being part of the study.

FWIW, the presenter/CEO/patient zero looks to be in poor shape. How much of a miracle drug can this be? Here, from 2019, you can see for yourself what kind of shape he was in. I don’t know how old he is, but I’d guess 70.


Steve Perry’s most recent presentation:


New research on GDF11:

Open Access Paper:

Systemic GDF11 attenuates depression-like phenotype in aged mice via stimulation of neuronal autophagy

Cognitive decline and mood disorders increase in frequency with age. Many efforts are focused on the identification of molecules and pathways to treat these conditions. Here, we demonstrate that systemic administration of growth differentiation factor 11 (GDF11) in aged mice improves memory and alleviates senescence and depression-like symptoms in a neurogenesis-independent manner. Mechanistically, GDF11 acts directly on hippocampal neurons to enhance neuronal activity via stimulation of autophagy. Transcriptomic and biochemical analyses of these neurons reveal that GDF11 reduces the activity of mammalian target of rapamycin (mTOR), a master regulator of autophagy. Using a murine model of corticosterone-induced depression-like phenotype, we also show that GDF11 attenuates the depressive-like behavior of young mice. Analysis of sera from young adults with major depressive disorder (MDD) reveals reduced GDF11 levels. These findings identify mechanistic pathways related to GDF11 action in the brain and uncover an unknown role for GDF11 as an antidepressant candidate and biomarker.


GDF11 implicated in depression

An international study involving McMaster University researchers has found that low levels of a certain blood protein may be a trigger for depression.

The growth differentiation factor 11 (GDF11) protein was found to regenerate neural stem cells, improve cognitive ability and reduce depression in mouse models. Analysis of blood samples from young adults with depression also revealed reduced GDF11 levels.

The research team included members from McMaster, the Paris-based Institut Pasteur, the Centre national de la recherche scientifique and the French National Institute of Health and Medical Research. The results were published in Nature Aging.

“GDF11 could be a complementary way to treat depression, as well as losing weight and keeping a healthy diet to stimulate autophagy. The sooner you treat depression the better,” said Flavio Kapczinski, co-principal investigator and professor emeritus of the Department of Psychiatry and Behavioural Neurosciences.

Full Paper (open access):


New research on GDF11:

GDF11 slows excitatory neuronal senescence and brain ageing by repressing p21

As a major neuron type in the brain, the excitatory neuron (EN) regulates the lifespan in C. elegans. How the EN acquires senescence, however, is unknown. Here, we show that growth differentiation factor 11 (GDF11) is predominantly expressed in the EN in the adult mouse, marmoset and human brain. In mice, selective knock-out of GDF11 in the post-mitotic EN shapes the brain ageing-related transcriptional profile, induces EN senescence and hyperexcitability, prunes their dendrites, impedes their synaptic input, impairs object recognition memory and shortens the lifespan, establishing a functional link between GDF11, brain ageing and cognition. In vitro GDF11 deletion causes cellular senescence in Neuro-2a cells. Mechanistically, GDF11 deletion induces neuronal senescence via Smad2-induced transcription of the pro-senescence factor p21. This work indicates that endogenous GDF11 acts as a brake on EN senescence and brain ageing.

Open Access: