Yesterday I finished J. Craig Venter’s autobiography, “A Life Decoded.” As you may have guessed from the clever title he was the first person to have his genome sequenced, an effort he led. Before that he led the charge on the first and second organism to be sequenced using his novel “EST Shotgun method.” Even if you’re not into biology or the politics of science, the book is inspiring and, taking into account all that he has been able to accomplish, it makes you want to borrow his mindset.
Intermittently he would add boxes that tie his life into what he knows about his DNA. A comment from Jaybe last weekend about his preference for serotonin pharmaceuticals as well as some trying events in my life this year incited me to share this one:
The attacks and setbacks I have experienced over the years would have plunged some people into profound depression. That is not to say I have not been down from time to time, but I have been fortunate that I have been mostly able to escape deep clinical depression. Is this because of my genes? A team led by Kay Wilhelm of Sydney’s St. Vincent’s Hospital and the University of New South Wales in Australia found that the influence of adversity on the onset of depression was significantly greater for those who inherited on chromosome 17 a short version of the serotonin transporter gene, known as 5-HTTLPR, from both parents.
The difference in length is in a part of the gene called the “activation sequence” that controls how much of the protein is made. As a result of having a shorter version, around one-fifth of the population makes less of a protein responsible for transporting the brain chemical serotonin, which plays a key role in mood and pain regulation, appetite, and sleep, and is affected by Prozac. They have an 80 percent chance of becoming clinically depressed if they experience three or more negative events in five years. Once again we have a study that undermines simpleminded genetic determinism: Brain chemistry depends on both genes and circumstances, on both biology and society.
The work also showed that those with a long version that gave them “genetic resilience” against depression had only a 30 percent chance of developing the mental illness, given similar circumstances. The remainder-about half of all people-have a mix of the two genotypes. Many other studies have linked the short version to anxiety-related personality traits including harm avoidance and neuroticism and increased experimentation with illegal drugs. Fortunately for me, I have two copies of the long form and more serotonin.
In addition to copious amounts of serotonin (which makes sense because he’s always sailing through big storms on the open ocean), I can tell by using the book as a portal into his brain and his obvious talent for research that he has tons of inductive reasoning skill. At least I think I can, whatever the case, it’s safe to say he found his calling.
My comrade at work tendered his Two Weeks Notice and will therefore be passing me the torch, that is, the dubious honor of being the “Most Disgruntled Employee in Show.” We had often contemplated that at the crux of our mutual dissatisfaction lie a dearth of the neurotransmitter and neurohormone 4-(2-aminoethyl)benzene-1,2-diol of the catecholamine family.
Dopamine, or Goofballs to you kids, is something that God assiduously spurns from our receptors. I will often liken the one operational dopamine receptor in my prefrontal cortex to the creaky screen door of a lone house on a dusty windswept plain. Comrade envisions greener pastures back in New Mexico, however, before bidding his adieu he seeks to refine our notion of dopamine function and I thought I would likewise share: