The geroscience hypothesis posits that therapies to retard biological processes of aging can prevent disease. To test such "geroprotective" therapies in humans, surrogate endpoints are needed for extension of disease-free lifespan. Methods to quantify biological aging could provide such surrogate endpoints, but different methods have not been systematically evaluated in the same humans. We studied seven measures of biological aging in 964 middle-aged humans in the Dunedin Study: telomere-length, three epigenetic-clocks, and three biomarker-composites. Agreement between these different measures of biological aging was low. We also tested agreement between measures and compared associations with outcomes that geroprotective therapies will seek to modify: physical functioning, cognitive decline, and subjective signs of aging. The 71-CpG epigenetic clock and the biomarker composites were consistently related to outcome metrics. Effect-sizes were modest. Quantification of biological aging is a young field. Next steps are to move toward systematic evaluation and refinement of methods.