Immune senescence is a predictable consequence of aging, and is responsible for many of the diseases of aging, including an increase in mortality from common respiratory infection, and cancer. The Thymus Regeneration, Immunorestoration and Insulin Mitigation (TRIIM) trial tested 9 white men between 51 and 65 years of age. It was led by immunologist Gregory Fahy, the chief scientific officer and co-founder of Intervene Immune in Los Angeles, and was approved by the US Food and Drug Administration in May 2015. It began a few months later at Stanford Medical Center in Palo Alto, California. The nine healthy volunteers took a cocktail of three common drugs — growth hormone and two diabetes medications — and on average shed 2.5 years of their biological ages, measured by analysing marks on a person’s genomes. The participants’ immune systems also showed signs of rejuvenation and age reversal. Remarkably, the rate of epigenetic age reversal was -1.6 years/year in the first 9 months of treatment, and accelerated to -6.5 years/year in the 9th-12th month.
In the TRIIM trial, the scientists measured blood samples fand found that blood-cell count was rejuvenated in each of the participants. The researchers also used magnetic resonance imaging (MRI) to determine the changes in the thymus, the gland responsible for the formation of T-cells. They found that in seven participants, thyme fatty atrophy had been replaced with regenerated thymus tissue.
Reversal of epigenetic aging and immunosenescent trends in humans, Gregory M. Fahy,Robert T. Brooke, James P. Watson, Zinaida Good
Aging Cell, Open Access, 08 September 2019
Epigenetic “clocks” can now surpass chronological age in accuracy for estimating biological age. Here, we use four such age estimators to show that epigenetic aging can be reversed in humans. Using a protocol intended to regenerate the thymus, we observed protective immunological changes, improved risk indices for many age‐related diseases, and a mean epigenetic age approximately 1.5 years less than baseline after 1 year of treatment (−2.5‐year change compared to no treatment at the end of the study). The rate of epigenetic aging reversal relative to chronological age accelerated from −1.6 year/year from 0–9 month to −6.5 year/year from 9–12 month. The GrimAge predictor of human morbidity and mortality showed a 2‐year decrease in epigenetic vs. chronological age that persisted six months after discontinuing treatment. This is to our knowledge the first report of an increase, based on an epigenetic age estimator, in predicted human lifespan by means of a currently accessible aging intervention.