Bioviva didn't succeed as originally envisaged, as a vehicle to bring human telomerase and follistatin gene therapy to the clinic; a recent article gave an outline of this history. At the moment I think few people are working on follistatin delivery, more is the pity, and the telomerase gene therapy banner has been taken up by another group. The original volunteer test subject, Liz Parrish, continues to perform a public service by publishing data on the outcome of her gene therapy - though I have to say that average telomere length as presently measured in sample of white blood cells is just about the least interesting of any measure one might propose to take following gene therapy with telomerase and follistatin.
Telomerase acts to lengthen telomeres, but average telomere length in immune cells is a terrible metric for age and tissue status. Average telomere length is an outcome of the pace at which cells are created from their stem cell populations, fresh with long telomeres, and the pace at which they divide, losing a little telomere length each time. In immune cells these behaviors are highly variable, greatly influenced by many transient health and environmental circumstances that have little to do with aging. Study after study shows immune cell telomere length to have a very poor correlation with age and age-related disease.
So instead, how about metrics of stem cell activity, or immune function, for example? The rationale for telomerase gene therapy is largely that it increases stem cell activity in tissue maintenance, and since it also reduces cancer risk in mice, one might suspect it is improving the ability of the immune system to destroy cancerous cells. Average telomere length on its own is interesting, but it cannot be used to claim rejuvenation, as is done here. It is too disconnected from meaningful metrics of aging, those that are actually closely tied to function and damage.
Before I underwent the therapy procedure, my white blood cell telomeres were measured in September, 2015 by SpectraCell's Texas laboratory, using a blood sample. They were determined to be unusually short, meaning that I was aging much faster than others my age. According to my telomeres, I was supposed to be in my mid-sixties. In March 2016, my telomeres were again measured by SpectraCell. I had already started at a disadvantage, which multiplied the anticipation anxiety. Thankfully, the results exceeded all my expectations. They showed that my telomeres had been extended from an initial 6.71kb to 7.33kb, meaning that my cells grew younger by about 20 years in only 6 months. The gene therapies had restored my telomeres in these cells to my normal age.
I hardly dared to hope there was room for improvement still. In 2018 I went again for testing at SpectraCell. My telomeres further increased from 7.33kb in 2016 to 8.12kb in 2018, equivalent to another decade of cellular rejuvenation. This outcome has exceeded all my expectations. First, because there have so far been no negative effects of my therapy. That is, no cancer, the alleged danger with activating the telomerase enzyme. But second, because my telomeres have continued to get longer without any additional treatment.
The same improvement was obtained following the muscle deterioration treatments: not only did my muscle mass increase after the myostatin inhibitor therapy, but continues to be robust 3 years after it took place. From pre-treatment to post treatment a growth in overall muscle mass and a reduction of intramuscular fat content was observed over a period of three years. This loss of intramuscular fat, also known as 'marbling', is associated with beneficial metabolic changes and improved musculature. My overall body weight did not decrease during this period. As my personal experience shows, a single treatment stimulated the telomerase and the myostatin inhibitor enzymes for at least 3 years after being administered, with no adverse effect. This can be a proof of concept that these two therapies, amply tested in animal models, are safe and efficient in humans.