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The supplement telomerase activator TA-65 (purified from Astragalus membranaceus) has been shown to retard cellular senescence, boost the aging immune system, and retard age-related symptoms. Lengthened telomeres retard aging, but because cancers often maintain longevity by lengthening telomeres, dietary telomerase activator might possibly increase tumorigenesis. This study investigated whether oral TA-65 effects the timing of onset and/or the incidence of skin cancers induced by UVB-irradiation and whether that possible effect is different if the oral supplementation is begun only after tumors are first detected clinically or if supplementation is begun before initiation of tumors as well as during and after the inciting UVB exposure. Three groups of ten Skh:1 hairless, nonpigmented mice exposed to UVB for twenty weeks were given (1) no supplementation, (2) TA-65 supplementation starting when the first UV-induced skin cancers were clinically observed, after which the UV exposure was terminated, and (3) TA-65 supplementation before, during, and after UV exposure (as more tumors subsequently appeared). Except for two time points when Group 3 had borderline or statistically more tumors ≥ 2mm per mouse, overall, there was no statistically significant difference in the time of onset, the incidence, or the tumor load of skin cancers with TA-65 with either timing, confirming the safety of this anti-aging supplement in this model of the most frequent human malignancy.

The Safety of Oral Telomerase Activator in UV-Induced Skin Cancer with A Review of Telomerase in Aging and Skin Carcinogenesis