Some items we've gotten from some colleagues in the last week or so. Here you can find the latest NJ Commission electronic newsletter, courtesy of Ben Barlyn. Again, let me assure you that, if you are planning a commission, Ben is a great guide for organizing meetings and materials. And he'd be glad to work with you, I'm happy to volunteer him. Keep the good things coming, Ben. . . . And below a devoted reader (with that rare combo of law degree and public affairs Master's) contributes to some points to an aspect of the technocorrections discussion we've had here:
One of the articles that I mentioned last week "DNA is Not Destiny" (Discover Magazine, October 2006) was good reading, distantly related to your favorite subject, "technocorrections." The article was about the chemical markers that switch particular genes on/off. The general term is epigenetics. Here's a good summary of the article, from the article itself:
The mind-set at the moment is that the information we inherit from our parents is in the form of DNA. Our experiment demonstrates that it's more than just DNA. In a sense, that's obvious, because what we inherit from our parents are chromosomes, and chromosomes are only 50 percent DNA. The other 50 percent is made up of protein molecules, and these proteins carry the epigenetic marks and information.
And what function does the epigenome perform?
[G]enes themselves need instructions for what to do, and where and when to do it. A human liver cell contains the same DNA as a brain cell, yet somehow it knows to code only those proteins needed for the functioning of the liver. Those instructions are found not in the letters of the DNA itself, but on it, in an array of chemical markers and switches, known collectively as the epigenome, that lie along the length of the double helix.
. . .
We commonly accept the notion that through our DNA we are destined to have particular body shapes, personalities and diseases. Some scholars even contend that the genetic code predetermines intelligence and is the root cause of many social ills, including poverty, crime and violence. "Gene as fate" has become the conventional wisdom. Through the study of epigenetics, that notion at last may be proved outdated.
The article says that diet, environment, and pre- and post-natal exposure to vitamins, toxins, etc. can alter the epigenome, affecting the _expression/suppression of genes related to disease, behavior and cognitive development. Moreover, epigenetic changes made in the parent generation can turn up several generations down the line, long after the original trigger for the change has been removed. Thus,
our diet, behavior and environmental surroundings today could have a far greater impact than imagined on the health of our distant descendants. . . . The logic applies backward as well as forward: Some of the disease patterns prevalent today may have deep epigenetic roots. [Marcus] Pembrey and several other researchers, for instance, have wondered whether the current epidemic of obesity, commonly blamed on the excesses of the current generation, may partially reflect lifestyles adopted by our forebears two or more generations back. Michael Meaney, who studies the impact of nurturing, likewise wonders what the implications of epigenetics are for social policy. He notes that early child-parent bonding is made more difficult by the effects of poverty, dislocation and social strife. Those factors can certainly affect the cognitive development of the children directly involved. Might they also affect the development of future generations through epigenetic signaling?
One of the experiments discussed in the article involved the “emotional” development of rats. Rats that were neglected as youngsters produced more of the stress hormone cortisol in startling/stressful situations. Consequently, they reacted “nervously.” Rats that were nurtured by attentive mothers were more likely to remain calm. The author notes that the genetic sequence silenced by the attentive mother rats has a close parallel in the human genome. According to Michael Meaney, a biologist at McGill University , “it’s just not going to make any sense if we don’t find this in humans as well. The story is going to be more complex that with the rats because we’ll have to take into account more social influences, but I’m convinced we’re going to find a connection.”
Meaney also notes that trichostatin A — a drug used to simulate the effects of good and bad parenting in the experiment — is chemically similar to the drug valproate, which is given to people as a mood stabilizer.
Thanks to both, and let me repeat how appreciative we are of anything that you think will contribute to our little discussion group here. Just hit "contact or contribute" on the right or send a comment. It will be very welcome.