Enhancing Human Ability in the 21st Century

The Economist recently published a video interview on pushing the limits of human ability in light of the 2012 London Olympic Games. Watch an interesting discussion on the limits of human ability and what it would take to surpass them.

The Top Genetic Enhancements already done in mammals

Whether we are talking about making people smarter or stronger or able to fly or whatever, we are talking about making changes to the complex systems that underpin human ability. Below is a quick canter through the top genetic enhancements that have already been done in mammals (and hence could presumably be done in humans).

1. The Doogie Mouse. Better memory through over expression of NMR2B. A very simple, yet good demonstration of how plastic our memory system is. Since then several other ways of enhancing memory genetically have been found, with slightly different effects on different types of memory, forgetting and side effects.

Tan, D. P., Q. Y. Liu, et al. (2006). "Enhancement of long-term memory retention and short-term synaptic plasticity in cbl-b null mice." Proceedings of the National Academy of Sciences of the United States of America 103(13): 5125-5130.

2. Color vision mice. Adding human photo pigment allows (at least females) to see new colors. This is extra interesting since it shows the brain can adapt to the signals from a new sense, at least when growing up with it.

Gerald H. Jacobs, Gary A. Williams, Hugh Cahill, Jeremy Nathans, Emergence of Novel Color Vision in Mice Engineered to Express a Human Cone Photopigment, Science 23 March 2007: Vol. 315. no. 5819, pp. 1723 - 1725

3. Methuselah mice. By reducing growth hormone levels long-lived dwarf mice can be produced. The current record holder survived 4 years 11 months and 3 weeks, while normal mice have a two year lifespan.

A. Bartke, H. Brown-Borg, J. Mattison, B. Kinney, S. Hauck, C. Wright, Prolonged longevity of hypopituitary dwarf mice. Exp. Gerontol. 36, 21-28 (2001) Bartke A, Brown-Borg H. Life extension in the dwarf mouse. Curr Top Dev Biol. 2004;63:189-225.

4. Monogamous voles. Normally non-monogamous voles can be turned monogamous (and more social) by changing the vassopressin V1a receptor.

Lim M. M., Wang Z., Olazábal D. E., Ren X., Terwilliger E. F. and Young L. J. 2004 Enhanced partner preference in a promiscuous species by manipulating the expression of a single gene. Nature 429, 754–757.

5. Regenerating MRL mice (OK, a case of accidental breeding rather than genetic engineering, and it involves at least 20 genes). These mice regenerate holes punched in their ears as well as some injuries to heart muscle.

Schuelke M, Wagner KR, Stolz LE, Hubner C, Riebel T, Komen W, Braun T., Tobin JF, Lee SJ. Myostatin mutation associated with gross muscle hypertrophy in a child. N Engl J Med 2004: 350: 2682–2688.

Lee SJ (2007) Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways. PLoS ONE 2(8)

6. The hard working monkeys. Work discipline through a blocked dopamine D2 gene. Monkeys tend to slack off until they get close to a reward they have to work for. If injected with a DNA construct that blocks the D2 receptor they worked at an even rate. This is likely less a case of workaholism and more a case of specific memory impairment for how rewarding situations look. Still, adjusting the dopamine system is likely to enable boosts of motivation.

Zheng Liu, Barry J. Richmond, Elisabeth A. Murray, Richard C. Saunders, Sara Steenrod, Barbara K. Stubblefield, Deidra M. Montague, and Edward I. Ginns, DNA targeting of rhinal cortex D2 receptor protein reversibly blocks learning of cues that predict reward, PNAS August 17, 2004 vol. 101 no. 33, 12336–12341

7. Anticancer mice. These mice (the result of a lucky mutation) have immune systems that kill cancer cells efficiently and can even help other mice through blood transfusions.

Cui Z, Willingham MC, Hicks AM, Alexander-Miller MA, Howard TD, Hawkins GA, Miller MS, Weir HM, Du W, DeLong CJ. Spontaneous regression of advanced cancer: identification of a unique genetically determined, age-dependent trait in mice. Proc Natl Acad Sci U S A. 2003 May 27;100(11):6682-7.

Hicks AM, Riedlinger G, Willingham MC, Alexander-Miller MA, Von Kap-Herr C, Pettenati MJ, Sanders AM, Weir HM, Du W, Kim J, Simpson AJG, Old LG, Cui Z. Transferable anticancer innate immunity in spontaneous regression/complete resistance mice. PNAS E-published May 8, 2006.

8. Antiobesity mice. These mice are protected from getting obese and diabetic from their diet by their lack of acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1). Their fat tissue can even reduce obesity and glucose buildup in other mice if transplanted. There are other strains protected from obesity by lack of other proteins, and a strain that have more adiponectin that put all excess fat into their blubber, remaining healthy despite turning very obese.

Smith SJ, et al. Obesity resistance and multiple mechanisms of triglyceride synthesis in mice lacking DGAT. Nat. Genet. 2000;25:87–90 

 

Chen HC, et al. Increased insulin and leptin sensitivity in mice lacking acyl CoA:diacylglylcerol acyltransferase 1. J. Clin. Invest. 2002;109:1049–1055. doi:10.1172/JCI200214672.

9. Marathon mice. These mice have more expression of PPARδ in their muscles, which makes them turn into type I (slow twitch) fibers that work well for long-distance running. The mice have more endurance and - even when not training - increased resistance to obesity.

Wang YX, Zhang CL, Yu RT, Cho HK, Nelson MC, et al. (2004) Regulation of Muscle Fiber Type and Running Endurance by PPARδ. PLoS Biol 2(10): e294

So what does this mean for the future

The Geo-Trade Blog believes that our relationship with technology and how it stretches our ability to perform in the world will be one of the key areas of advance in the 21st Century. In fact, how we answer the following questions will be key to determining the parameters: What does the future, near and far, hold for humans? Is enhancement the next stage of evolution? Should any limits be imposed? And if so, how?