Can someone explain the point of all these anti-bot systems that block me but happily let ChatGPT through when I ask it to summarize the very same website?

Several people asked to see before and after, rather than just the treated side versus placebo. The difference looks pretty striking. But this shows the result of the entire regimen: VEGF gene therapy, minoxidil, finasteride, dutasteride, red light and scalp care. The treated-side vs placebo-side comparison helps assess what VEGF may have added on top of everything else.

They say gene therapies are expensive. For the first time in history, a drug that inhibits myostatin activation has been approved. On September 11, the FDA approved for SMA ISEMBYLD — apitegromab, developed by Scholar Rock. Apitegromab is a monoclonal antibody that binds inactive forms of myostatin and prevents them from becoming activated. This is a genuinely historic event. After decades of failed development programs, the myostatin pathway has finally produced an approved drug. At first glance, it may seem that we now have a practical treatment for preserving and growing muscle — one that will almost certainly be explored off-label. A therapy capable of preserving or increasing functional muscle mass with minimal physical effort and an acceptable safety profile would be a true Holy Grail. But there is a small catch: the price and the treatment format. Apitegromab is administered intravenously once every four weeks. For an adult weighing 80 kg, the drug alone would cost approximately: $70,000 per infusion. Thirteen infusions per year: nearly $1 million annually. And that is only the cost of the drug, excluding the infusion center, laboratory testing, and medical supervision. Antibody-based drugs in their current format are still far too expensive and inconvenient. Monthly intravenous infusions with an annual drug bill approaching $1 million are not a realistic mass-market solution. Gene therapies would be much affordable

Muscle-growth plateaus: what if the limitation isn’t just the growth signal? Could further muscle growth be constrained not only by the stimulus to grow, but also by the tissue’s capacity to support that growth? One possibility worth investigating is whether vascular adaptation can become a limiting factor under some conditions. Our mouse study explored a question: what happens when we combine stimulation of muscle growth with stimulation of vascular development? We administered VEGF plasmid gene therapy before intramuscular AAV-follistatin. Attached figure shows distinct patterns. AAV-follistatin alone: mean muscle fiber diameter was 36.2 μm versus 25.8 μm in controls—about 40% larger. CD31+ vessel counts were 35 versus 30 per microscopic field, remaining close to control. VEGF plasmid alone: vessel counts reached 68 per field, while mean fiber diameter was 24.4 μm, compared with 25.8 μm in controls. The higher vessel count was not accompanied by larger fibers. The combination showed both: the largest mean fiber diameter: 40.2 μm versus 36.2 μm with follistatin alone, approximately 11% greater. Vessel counts were 70 versus 35 per field—twice as many. The combination was associated not only with more vessels, but also with larger muscle fibers than follistatin alone. That pattern is consistent with a hypothesis worth testing: vascular adaptation may influence how much growth a muscle can achieve—not merely accompany it

5 steps to make any cancer curable: 1. early complex diagnostics 2. maximize individualization 3. maximize combinations 4. do all of the above fast 5. repeat The tragedy is that cancer might already be curable, but we fail as a society to address it because we’re too busy optimizing likes and views on social media. Cancer changes. Measure it, adapt the treatment, hit it again. Repeat until it’s gone. Do it with no delay. We should start offering individualized combinatory cancer solutions in Próspera.

There’s one organ I’d keep our VEGF plasmid away from: the eye. Naturally, that’s where ER-100 is starting 😅 @davidasinclair, when do human trials move beyond the eye? Maybe our approach could help lower the AAV bill starting with muscle?

We might be close to a breakthrough in the gene therapy field. Manufacturing AAV vectors is expensive, and gene therapies can cost millions of dollars. Zolgensma, for example, launched in the US at a price of $2.125 million for a one-time treatment. At the same time AAV therapies carry risks, including serious liver injury. Our approach is to prepare the muscle before administering AAV: first, stimulate capillary network development using VEGF plasmid gene therapy, then administer AAV-follistatin intramuscularly. In our mouse study, following this preparation, we observed approximately twice as much follistatin in muscle at the same AAV dose. The muscle-to-liver transgene expression ratio, measured at the mRNA level, was 2.6-fold higher than with AAV monotherapy. If we can achieve the same therapeutic effect with half the AAV dose in clinical trials, this could be a breakthrough for muscle-targeted gene therapies: less vector per patient, potentially reducing both manufacturing costs and dose-related risks. Much more to come.

“Again, extraordinary claims require extraordinary evidence.” 100% agree. Partial reprogramming ≠ rejuvenation. Failure to recognize this distinction has already led the field to waste billions of dollars on overhyped projects.

Interval training can raise VEGF and improve muscle capillarization. It is accessible, and at my age I still plan to get these benefits mainly through exercise, rather than rushing to use gene therapies on myself even though my company develops them. I have said this many times: first, we should get everything we can from exercise, sleep, nutrition, and risk-factor control. But only while we can. The fact that exercise is available today does not mean it will always be available. A joint starts hurting, then an injury takes you out for a few weeks, followed by an infection, surgery, or another illness. These breaks add up. You lose muscle and endurance, returning becomes harder, and the risk of another injury rises. At some point, it is no longer about discipline. A person may want to train, but their body cannot tolerate enough load. That is why we need exercise mimetics: technologies that preserve some benefits of exercise, such as capillarization and muscle function, when proper training is temporarily or permanently impossible. Not to replace exercise in healthy people, but to preserve its benefits when the body needs them most.