Retatrutide isn’t for fat loss. That’s just where people noticed it first.
What’s actually happening here is much more interesting.
Retatrutide targets three key pathways at once:
GLP-1 for appetite control,
GIP for metabolic regulation,
and glucagon for energy expenditure.
Most drugs in this category stop at reducing calories in.
This one also increases calories out.
That changes the entire equation.
And the data supports that this goes far beyond weight loss.
In human trials, liver fat reduction was one of the most striking outcomes. Between 43% and 100% of participants achieved at least a 50% reduction in liver fat, and up to 93% reached near-normal levels. At higher doses, by week 48, 89–93% of participants had normalized liver fat levels.
That’s not cosmetic. That’s organ-level reversal.
Glucose metabolism shows the same pattern. Around 72% of participants with prediabetes returned to normal glycemic levels, compared to just 22% in the placebo group. That’s more than a threefold difference.
Blood pressure also dropped significantly, with roughly 30–40% of participants able to discontinue at least one antihypertensive medication.
So what you’re seeing is not just weight reduction.
You’re seeing improvements in:
insulin sensitivity,
fat oxidation,
ectopic fat reduction,
and overall energy partitioning.
This is metabolic reprogramming.
Which leads to a more interesting question.
What happens when you apply something like this to someone who is already lean?
Not more weight loss.
But potentially better fuel utilization, cleaner metabolic signaling, and reduced hidden risk factors like liver fat or early insulin resistance.
That’s where this is going.
Not just treating obesity,
but optimizing metabolism.
But there’s a constraint most people ignore.
If your baseline is off,
micronutrients, sleep, stress, recovery,
you’re not upgrading performance.
You’re amplifying dysfunction.
Peptides don’t fix broken systems. They scale whatever is already there.
Retatrutide is not the end of weight loss drugs.
It’s the beginning of precision metabolic control.
What’s actually happening here is much more interesting.
Retatrutide targets three key pathways at once:
GLP-1 for appetite control,
GIP for metabolic regulation,
and glucagon for energy expenditure.
Most drugs in this category stop at reducing calories in.
This one also increases calories out.
That changes the entire equation.
And the data supports that this goes far beyond weight loss.
In human trials, liver fat reduction was one of the most striking outcomes. Between 43% and 100% of participants achieved at least a 50% reduction in liver fat, and up to 93% reached near-normal levels. At higher doses, by week 48, 89–93% of participants had normalized liver fat levels.
That’s not cosmetic. That’s organ-level reversal.
Glucose metabolism shows the same pattern. Around 72% of participants with prediabetes returned to normal glycemic levels, compared to just 22% in the placebo group. That’s more than a threefold difference.
Blood pressure also dropped significantly, with roughly 30–40% of participants able to discontinue at least one antihypertensive medication.
So what you’re seeing is not just weight reduction.
You’re seeing improvements in:
insulin sensitivity,
fat oxidation,
ectopic fat reduction,
and overall energy partitioning.
This is metabolic reprogramming.
Which leads to a more interesting question.
What happens when you apply something like this to someone who is already lean?
Not more weight loss.
But potentially better fuel utilization, cleaner metabolic signaling, and reduced hidden risk factors like liver fat or early insulin resistance.
That’s where this is going.
Not just treating obesity,
but optimizing metabolism.
But there’s a constraint most people ignore.
If your baseline is off,
micronutrients, sleep, stress, recovery,
you’re not upgrading performance.
You’re amplifying dysfunction.
Peptides don’t fix broken systems. They scale whatever is already there.
Retatrutide is not the end of weight loss drugs.
It’s the beginning of precision metabolic control.
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Your job is aging your face. Just not the way you think.
We like to blame skincare, genetics, or “getting older.”
But your face is a data log. And your job is one of the biggest inputs.
I came across this dataset showing how different professions correlate with facial aging. Not perceived stress. Not income. Actual facial age acceleration.
Here’s the pattern:
Athletes: +1.3 years
Service workers: +2.1 years
Sales: +2.9 years
Clerical: +3.6 years
Managers: +4.3 years
Professionals: +5.1 years
Scientists & educators: +6.4 years
Let that sink in.
The people studying aging… look the oldest.
What’s actually going on
This isn’t about the job title. It’s about what the job does to your biology.
We like to blame skincare, genetics, or “getting older.”
But your face is a data log. And your job is one of the biggest inputs.
I came across this dataset showing how different professions correlate with facial aging. Not perceived stress. Not income. Actual facial age acceleration.
Here’s the pattern:
Athletes: +1.3 years
Service workers: +2.1 years
Sales: +2.9 years
Clerical: +3.6 years
Managers: +4.3 years
Professionals: +5.1 years
Scientists & educators: +6.4 years
Let that sink in.
The people studying aging… look the oldest.
What’s actually going on
This isn’t about the job title. It’s about what the job does to your biology.
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People Are Starting to Wake Up to Vilon—Here’s Why
Vilon (Lys-Glu), a tiny two-amino-acid Khavinson dipeptide, is quietly gaining traction in biohacking and longevity circles. While the broader peptide wave is exploding in 2026, Vilon stands out for its foundational, gene-level effects rather than hype-driven stimulation.
Why the Buzz Is Growing
Powerful Immune & Thymus Support
As a thymomimetic, it promotes thymocyte proliferation, T-cell maturation, and reactivates aged immune cells through chromatin deheterochromatinization. This helps restore immune function in aging, stress, and metabolic models.
Longevity & Anti-Tumor Effects
Animal studies show 20–40% lifespan extension in mice, reduced spontaneous tumor incidence, and better cellular repair. It modulates gene expression and protein synthesis for healthier aging.
Tissue Regeneration
Supports wound healing, intestinal epithelium repair, retinal and neuronal recovery, and reduces inflammation.
Neuroendocrine Benefits
Lowers elevated prolactin in aging models, aiding sexual function, libido, and hypothalamic balance. Anecdotes highlight better energy, recovery, and performance (less DOMS, enhanced training).
Metabolic Edge
A 2006 human RCT in type 1 diabetes patients demonstrated improved coagulation, fibrinolysis, and reduced complications.
Vilon (Lys-Glu), a tiny two-amino-acid Khavinson dipeptide, is quietly gaining traction in biohacking and longevity circles. While the broader peptide wave is exploding in 2026, Vilon stands out for its foundational, gene-level effects rather than hype-driven stimulation.
Why the Buzz Is Growing
Powerful Immune & Thymus Support
As a thymomimetic, it promotes thymocyte proliferation, T-cell maturation, and reactivates aged immune cells through chromatin deheterochromatinization. This helps restore immune function in aging, stress, and metabolic models.
Longevity & Anti-Tumor Effects
Animal studies show 20–40% lifespan extension in mice, reduced spontaneous tumor incidence, and better cellular repair. It modulates gene expression and protein synthesis for healthier aging.
Tissue Regeneration
Supports wound healing, intestinal epithelium repair, retinal and neuronal recovery, and reduces inflammation.
Neuroendocrine Benefits
Lowers elevated prolactin in aging models, aiding sexual function, libido, and hypothalamic balance. Anecdotes highlight better energy, recovery, and performance (less DOMS, enhanced training).
Metabolic Edge
A 2006 human RCT in type 1 diabetes patients demonstrated improved coagulation, fibrinolysis, and reduced complications.
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If you ever wanted to know how body fat % impacts longevity and how caloric restriction impacts your risk for cancer.
This podcast with the world renowned Sr Joel Fuhrman, the personal doctor to the superstars in Hollywood, will give you incredible insights.
https://yt.openinapp.co/olt5b
This podcast with the world renowned Sr Joel Fuhrman, the personal doctor to the superstars in Hollywood, will give you incredible insights.
https://yt.openinapp.co/olt5b
yt.openinapp.co
Longevity Doctor: Easy Fixes To Slow Aging & Live Healthier (Works For Everyone)
@drfuhrman has practised nutritional medicine for over 35 years, and this conversation reveals why most protein and performance advice is wrong, how slowing your metabolism extends lifespan, and why eating more vegetables matters more than exercise for longevity.…
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Botox may do more than freeze wrinkles. It may drop your orgasms.
A study looked at 36 women.
24 received Botox in the face.
12 received other cosmetic treatments as controls.
The result?
The Botox group showed a significant drop in the “orgasm” domain of the Female Sexual Function Index.
The control group did not.
The theory is actually fascinating:
Facial expressions may not just communicate pleasure to someone else.
They may be part of how the brain feels pleasure in the first place.
So when Botox reduces the ability to fully express certain emotions, it may also reduce the intensity of the emotion itself.
Your face is not just a cosmetic surface.
It is part of your nervous system, your emotional feedback loop, and potentially even your sexual response.
A study looked at 36 women.
24 received Botox in the face.
12 received other cosmetic treatments as controls.
The result?
The Botox group showed a significant drop in the “orgasm” domain of the Female Sexual Function Index.
The control group did not.
The theory is actually fascinating:
Facial expressions may not just communicate pleasure to someone else.
They may be part of how the brain feels pleasure in the first place.
So when Botox reduces the ability to fully express certain emotions, it may also reduce the intensity of the emotion itself.
Your face is not just a cosmetic surface.
It is part of your nervous system, your emotional feedback loop, and potentially even your sexual response.
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What if LDL cholesterol becomes a one-time treatment?
Eli Lilly’s newly acquired Verve program is one of the most important things happening in cardiovascular medicine.
The idea is simple but massive:
Instead of taking cholesterol medication for life, edit the gene in the liver that controls LDL production.
One infusion.
Potentially long-term LDL reduction.
Not a daily pill.
Not a monthly injection.
In early Phase 1 data, VERVE-102 showed mean LDL reductions around 50%+, with some participants seeing reductions close to 70%. The therapy targets PCSK9, the same pathway already validated by existing cholesterol drugs, but through gene editing rather than repeated dosing.
Important nuance: this is still early. Small trial. High-risk patients. Long-term safety and durability still need to be proven.
But the direction is clear.
Cardiovascular disease has always been treated as chronic management.
Eli Lilly’s newly acquired Verve program is one of the most important things happening in cardiovascular medicine.
The idea is simple but massive:
Instead of taking cholesterol medication for life, edit the gene in the liver that controls LDL production.
One infusion.
Potentially long-term LDL reduction.
Not a daily pill.
Not a monthly injection.
In early Phase 1 data, VERVE-102 showed mean LDL reductions around 50%+, with some participants seeing reductions close to 70%. The therapy targets PCSK9, the same pathway already validated by existing cholesterol drugs, but through gene editing rather than repeated dosing.
Important nuance: this is still early. Small trial. High-risk patients. Long-term safety and durability still need to be proven.
But the direction is clear.
Cardiovascular disease has always been treated as chronic management.
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Yes, Coke Zero is not good for your health - but it’s much better than regular Coke - by how much - watch till the end.
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The Peptide Quietly Showing Up Alongside Cancer Research in Europe
Most people in health optimization know peptides for recovery, fat loss, or longevity.
But one peptide that quietly keeps appearing in European integrative and oncology-adjacent conversations is not for aesthetics or performance.
It’s about the immune system.
I’m talking about Thymosin Alpha-1 (TA-1).
TA-1 is a naturally occurring peptide produced by the thymus gland, the organ responsible for “training” T-cells, one of the key players in immune defense. As we age, thymus activity declines, which is one of the reasons immune resilience decreases over time. TA-1 has been researched for decades as an immune modulator, meaning it may help restore or optimize immune signaling rather than simply “boost” immunity.
What caught my attention is how often TA-1 appears alongside conventional cancer therapies in research settings across Europe and globally. Not as a replacement for treatment, but as an adjunct being studied to potentially support immune function, treatment tolerance, and outcomes.
Some of the strongest research signals have been seen in:
• Non-small cell lung cancer
• Melanoma
• Liver cancer (hepatocellular carcinoma)
• Patients undergoing chemotherapy or immunotherapy support
In several studies, TA-1 has been associated with:
• Better immune cell activity (T-cells + NK cells)
• Reduced chemotherapy-related toxicity and infections
• Improved treatment tolerance and quality of life
• Potential synergistic effects with immunotherapy in selected cancers
Importantly: this is not a miracle cure, and the evidence is still evolving. Most researchers view TA-1 as a promising immune-supportive therapy that may complement standard oncology care, not replace it. Ongoing clinical trials are still trying to answer where it truly adds value and for whom.
Most people in health optimization know peptides for recovery, fat loss, or longevity.
But one peptide that quietly keeps appearing in European integrative and oncology-adjacent conversations is not for aesthetics or performance.
It’s about the immune system.
I’m talking about Thymosin Alpha-1 (TA-1).
TA-1 is a naturally occurring peptide produced by the thymus gland, the organ responsible for “training” T-cells, one of the key players in immune defense. As we age, thymus activity declines, which is one of the reasons immune resilience decreases over time. TA-1 has been researched for decades as an immune modulator, meaning it may help restore or optimize immune signaling rather than simply “boost” immunity.
What caught my attention is how often TA-1 appears alongside conventional cancer therapies in research settings across Europe and globally. Not as a replacement for treatment, but as an adjunct being studied to potentially support immune function, treatment tolerance, and outcomes.
Some of the strongest research signals have been seen in:
• Non-small cell lung cancer
• Melanoma
• Liver cancer (hepatocellular carcinoma)
• Patients undergoing chemotherapy or immunotherapy support
In several studies, TA-1 has been associated with:
• Better immune cell activity (T-cells + NK cells)
• Reduced chemotherapy-related toxicity and infections
• Improved treatment tolerance and quality of life
• Potential synergistic effects with immunotherapy in selected cancers
Importantly: this is not a miracle cure, and the evidence is still evolving. Most researchers view TA-1 as a promising immune-supportive therapy that may complement standard oncology care, not replace it. Ongoing clinical trials are still trying to answer where it truly adds value and for whom.
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After almost a year of the Hack You podcast and close to 50 of the world’s leading experts, few topics have created more debate than protein intake and fasting.
Over the past months, I’ve spent time reassessing both - not just what is “optimal,” but what is optimal depending on age, goals, and context. I wanted to step back from opinions and get closer to evidence.
That made sitting down with Alan Aragon especially valuable. Alan is widely considered one of the world’s leading evidence-based nutrition experts, and this episode brought real clarity on protein, fasting, longevity, and what actually matters.
Exactly the kind of conversation I wanted the Hack You podcast to create.
Great energy, free-flowing discussion, and practical takeaways.
Latest episode out now - enjoy.
https://youtu.be/t9RTWyOgL3w?si=liYfV0C8e4NKzvHb
Over the past months, I’ve spent time reassessing both - not just what is “optimal,” but what is optimal depending on age, goals, and context. I wanted to step back from opinions and get closer to evidence.
That made sitting down with Alan Aragon especially valuable. Alan is widely considered one of the world’s leading evidence-based nutrition experts, and this episode brought real clarity on protein, fasting, longevity, and what actually matters.
Exactly the kind of conversation I wanted the Hack You podcast to create.
Great energy, free-flowing discussion, and practical takeaways.
Latest episode out now - enjoy.
https://youtu.be/t9RTWyOgL3w?si=liYfV0C8e4NKzvHb
YouTube
Common Nutrition Lies Killing Your Muscle Growth & Fat Loss (Fix These Now) (E028)
The narrative telling you to lower protein for longevity is backwards. Alan explains why protein is the strongest macronutrient for appetite control, how higher protein wins in every controlled study for body composition and metabolic health, and why food…
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The newest trend is to reverse biological age. Kris Gethin has impacted the lives of millions of people and shares in this episode how his routine looks like.
https://youtu.be/uTyOGOPejr4?si=OVvoIrOQ5Z5YvnRi
https://youtu.be/uTyOGOPejr4?si=OVvoIrOQ5Z5YvnRi
YouTube
How I Reversed My Biological Age By 6 Years (The Complete System) (E029)
@krisgethin built the DTP training program, a high-rep low-rep pyramid approach, after injuries forced him away from heavy lifting, it became massively successful because it worked for his body.
His biggest discovery: reversing biological age came from…
His biggest discovery: reversing biological age came from…
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The 31 year old that reduced his biological age by 20 years to 11 ‼️years and wrote 10 books about it.
Latest Hack You episode out now:
https://youtu.be/_qTY-jp6LaE?si=7GbkWK2YqI8e4lXx
Latest Hack You episode out now:
https://youtu.be/_qTY-jp6LaE?si=7GbkWK2YqI8e4lXx
YouTube
31 Years Old But Biologically In My Teens (Here's Exactly How)
@SiimLand reversed his biological age from 31 to low double digits, but he's not obsessing over the metrics most people focus on.
He explains which genes actually matter for longevity, why blood markers tell a better story than genetics, and the surprising…
He explains which genes actually matter for longevity, why blood markers tell a better story than genetics, and the surprising…
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Magnesium might be one of the most overlooked nutrients in healthy aging.
Emerging research suggests that low magnesium status is linked to many of the biological processes associated with aging, including:
• Telomere shortening
• Chronic inflammation
• Stem cell exhaustion
• Cellular senescence (“zombie cells”)
• Mitochondrial dysfunction
• Impaired cellular communication
• Dysregulated nutrient sensing
• Reduced autophagy (the body’s cellular recycling system)
• Loss of proteostasis (protein quality control)
• Epigenetic alterations
• Gut microbiome imbalance
While magnesium isn’t a cure-all, it’s a critical cofactor in 300+ enzymatic reactions, supporting energy production, DNA repair, muscle and nerve function, and metabolic health.
The challenge? Many people don’t consume enough magnesium, and factors such as chronic stress, certain medications, gastrointestinal disorders, and highly processed diets can further reduce magnesium status.
Small deficiencies sustained over years may have larger consequences than we appreciate.
Reference: PMID: 38398820
Emerging research suggests that low magnesium status is linked to many of the biological processes associated with aging, including:
• Telomere shortening
• Chronic inflammation
• Stem cell exhaustion
• Cellular senescence (“zombie cells”)
• Mitochondrial dysfunction
• Impaired cellular communication
• Dysregulated nutrient sensing
• Reduced autophagy (the body’s cellular recycling system)
• Loss of proteostasis (protein quality control)
• Epigenetic alterations
• Gut microbiome imbalance
While magnesium isn’t a cure-all, it’s a critical cofactor in 300+ enzymatic reactions, supporting energy production, DNA repair, muscle and nerve function, and metabolic health.
The challenge? Many people don’t consume enough magnesium, and factors such as chronic stress, certain medications, gastrointestinal disorders, and highly processed diets can further reduce magnesium status.
Small deficiencies sustained over years may have larger consequences than we appreciate.
Reference: PMID: 38398820
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The scientist who discovered BPC-157 still takes it.
After more than 30 years researching BPC-157, Dr. Predrag Sikirić reportedly still uses it every day.
Interestingly, he doesn’t inject it.
He reportedly prefers the oral form, mixes it with water instead of swallowing the capsule whole, and takes it several times per day based on what he believes is a ~6-hour duration of action.
An interesting insight from the person who has studied BPC-157 longer than anyone else.
After more than 30 years researching BPC-157, Dr. Predrag Sikirić reportedly still uses it every day.
Interestingly, he doesn’t inject it.
He reportedly prefers the oral form, mixes it with water instead of swallowing the capsule whole, and takes it several times per day based on what he believes is a ~6-hour duration of action.
An interesting insight from the person who has studied BPC-157 longer than anyone else.
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Dream Bigger - Demand More than you think you deserve.
Why?
We overestimate the social cost of rejection. Most people assume a “no” will be awkward or damaging. In reality, people move on within seconds.
We underestimate how often people say yes. Studies by social psychologist Vanessa Bohns found that people predict far fewer people will agree to requests than actually do.
We experience the “liking gap.” After meeting someone, we usually think they liked us less than they actually did. Our internal perception is more negative than reality.
Every rejection reduces fear. The brain quickly adapts. After hearing “no” repeatedly, rejection loses its emotional impact, making you more confident and more likely to take opportunities.
Life rewards asking. Investors, jobs, partnerships, mentors, discounts, introductions, podcasts, and collaborations often happen because someone simply asked.
Why?
We overestimate the social cost of rejection. Most people assume a “no” will be awkward or damaging. In reality, people move on within seconds.
We underestimate how often people say yes. Studies by social psychologist Vanessa Bohns found that people predict far fewer people will agree to requests than actually do.
We experience the “liking gap.” After meeting someone, we usually think they liked us less than they actually did. Our internal perception is more negative than reality.
Every rejection reduces fear. The brain quickly adapts. After hearing “no” repeatedly, rejection loses its emotional impact, making you more confident and more likely to take opportunities.
Life rewards asking. Investors, jobs, partnerships, mentors, discounts, introductions, podcasts, and collaborations often happen because someone simply asked.
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Latest Hack You Episodes with the personal doctor of US President's including Bill Clinton - Sean O'Mara MD
Visceral Fat, Stress and why people slap each other on the butt 🐒
https://youtu.be/-xuN6sM93aY?si=ygaJXwfLh8sHQqZY
Visceral Fat, Stress and why people slap each other on the butt 🐒
https://youtu.be/-xuN6sM93aY?si=ygaJXwfLh8sHQqZY
YouTube
How To Lose Visceral Fat So Fast It Feels Like Cheating
@DrSeanOMara spent years studying visceral fat through MRI scans and discovered the uncomfortable truth: most people have zero awareness they're filled with disease because it doesn't show on the outside. Distance runners look shredded, but their internal…
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If you ever thought of going in to Ketosis - but didn’t want to fast for 3+ days.
This episode is for you.
Exogenous ketones and their benefits explained:
https://youtu.be/SX8b4DKjprU?si=oHBfFtC8zJ3S9Ea9
This episode is for you.
Exogenous ketones and their benefits explained:
https://youtu.be/SX8b4DKjprU?si=oHBfFtC8zJ3S9Ea9
YouTube
The Keto Expert: Improve Fat Loss & Muscle Growth By Eating MORE (Not Less)
Latt Mansor (@ketone-iq) has a PhD in physiology from Oxford studying metabolic flexibility, and he discovered something uncomfortable about himself: he was skinny fat at 26% body fat and nothing he did worked until he did the opposite.
He breaks down why…
He breaks down why…
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What is ER-100 and what does it have to do with aging?
ER-100 is an experimental gene therapy designed to partially reprogram cells toward a younger biological state.
It uses three transcription factors, OCT4, SOX2 and KLF4 (OSK), to change how certain genes are expressed without changing the underlying DNA sequence.
Why is this interesting?
As we age, our epigenome changes. Think of DNA as the hardware and the epigenome as the software controlling how that hardware operates. Over time, some of these instructions become altered and cells can lose aspects of their youthful function.
Partial epigenetic reprogramming asks a fascinating question:
Can we reset some of these instructions and make an old cell function younger again?
Preclinical research using OSK has shown restoration of more youthful gene expression patterns and improvements in function in aged or damaged retinal cells.
ER-100 is now being tested in humans, initially for optic nerve diseases including glaucoma. The first goal is to establish safety, not to treat aging.
ER-100 is an experimental gene therapy designed to partially reprogram cells toward a younger biological state.
It uses three transcription factors, OCT4, SOX2 and KLF4 (OSK), to change how certain genes are expressed without changing the underlying DNA sequence.
Why is this interesting?
As we age, our epigenome changes. Think of DNA as the hardware and the epigenome as the software controlling how that hardware operates. Over time, some of these instructions become altered and cells can lose aspects of their youthful function.
Partial epigenetic reprogramming asks a fascinating question:
Can we reset some of these instructions and make an old cell function younger again?
Preclinical research using OSK has shown restoration of more youthful gene expression patterns and improvements in function in aged or damaged retinal cells.
ER-100 is now being tested in humans, initially for optic nerve diseases including glaucoma. The first goal is to establish safety, not to treat aging.
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