Steve Horvath decided to try it on his own (not part of the study) but without HGH, and he hasn’t gotten the same results as the people in the study who are using HGH.
I’m interested to know more about what Dr. Horvath tried and found. Do you happen to have details?
I feel like I’m misunderstanding something, because I would expect that he doesn’t get the same results if he doesn’t take the treatment that’s hypothesized in the study to result in thymus regeneration (i.e. GH).
From the TRIIM paper (emphasis mine):
The purpose of the TRIIM trial was to investigate the possibility of using recombinant human growth hormone (rhGH) to prevent or reverse signs of immunosenescence in a population of 51‐ to 65‐year‐old putatively healthy men, which represents the age range that just precedes the collapse of the TCR repertoire. rhGH was used based on prior evidence that growth hormone (GH) has thymotrophic and immune reconstituting effects in animals (Kelley et al., 1986) and human HIV patients (Napolitano et al., 2008; Plana et al., 2011). Because GH‐induced hyperinsulinemia (Marcus et al., 1990) is undesirable and might affect thymic regeneration and immunological reconstitution, we combined rhGH with both dehydroepiandrosterone (DHEA) and metformin in an attempt to limit the “diabetogenic” effect of GH (Fahy, 2003, 2010; Weiss, Villareal, Fontana, Han, & Holloszy, 2011). DHEA has many effects, in both men and women, that oppose deleterious effects of normal aging (Cappola et al., 2009; Forti et al., 2012; Shufelt et al., 2010; Weiss et al., 2011). Metformin is a powerful calorie restriction mimetic in aging mice (Dhahbi, Mote, Fahy, & Spindler, 2005) and has been proposed as a candidate for slowing aging in humans (Barzilai, Crandall, Kritchevsky, & Espeland, 2016). Neither DHEA (Riley, Fitzmaurice, & Regelson, 1990) nor metformin are known to have any thymotrophic effects of their own.