Raymond C. Kurzweil

The Law of Accelerating Returns

An analysis of the history of technology shows that technological change is exponential, contrary to the common-sense “intuitive linear” view. So we won’t experience 100 years of progress in the 21st century — it will be more like 20,000 years of progress (at today’s rate). The “returns,” such as chip speed and cost-effectiveness, also increase exponentially. There’s even exponential growth in the rate of exponential growth. Within a few decades, machine intelligence will surpass human intelligence, leading to The Singularity — technological change so rapid and profound it represents a rupture in the fabric of human history. The implications include the merger of biological and nonbiological intelligence, immortal software-based humans, and ultra-high levels of intelligence that expand outward in the universe at the speed of light.

Bridges to Life

The future of aging and human life extension begins today, using presently available tools, but will be increasingly shaped and accelerated by ongoing breakthroughs in biotechnology, nanotechnology and artificial intelligence in the years ahead. These developing technologies should allow many to journey over what can be seen as three bridges to ever-improving life and health expectancy, such that some who survive as a result of “bridge one” may be able to benefit from “bridge two” and even from “bridge three.” We begin our perspective on the future of aging with a brief overview of a sampling of present approaches to life extension (“bridge one”) and then explain why biotechnology (“bridge two”) and nanotechnology plus artificial intelligence (“bridge three”) might allow many of us to benefit from remarkably extended lifespans in the future.

Mutator/hypermutable fetal/juvenile metakaryotic stem cells and human colorectal carcinogenesis

Adult age-specific colorectal cancer incidence rates increase exponentially from maturity, reach a maximum, then decline in extreme old age. Armitage and Doll (1) postulated that the exponential increase resulted from “n” mutations occurring throughout adult life in normal “cells at risk” that initiated the growth of a preneoplastic colony in which subsequent “m” mutations promoted one of the preneoplastic “cells at risk” to form a lethal neoplasia. We have reported cytologic evidence that these “cells at risk” are fetal/juvenile organogenic, then preneoplastic metakaryotic stem cells. Metakaryotic cells display stem-like behaviors of both symmetric and asymmetric nuclear divisions and peculiarities such as bell shaped nuclei and amitotic nuclear fission that distinguish them from embryonic, eukaryotic stem cells. Analyses of mutant colony sizes and numbers in adult lung epithelia supported the inferences that the metakaryotic organogenic stem cells are constitutively mutator/hypermutable and that their contributions to cancer initiation are limited to the fetal/juvenile period. We have amended the two-stage model of Armitage and Doll and incorporated these several inferences in a computer program CancerFit v.5.0. We compared the expectations of the amended model to adult (15–104 years) age-specific colon cancer rates for European-American males born 1890–99 and observed remarkable concordance. When estimates of normal colonic fetal/juvenile APC and OAT gene mutation rates (∼2–5 × 10−5 per stem cell doubling) and preneoplastic colonic gene loss rates (∼8 × 10−3) were applied, the model was in accordance only for the values of n = 2 and m = 4 or 5.