Live-Blogging the APA: Better Aging Through Telomerase
How a 'junk' genetic region keeps us young, and a street drug as antidepressant.
Posted May 29, 2013
Yesterday, I wrote that Dr. Smalls' lecture on Alzheimer's disease turned out to be a ringing endorsement for a few common-sense lifestyle choices: getting enough exercise, eating well, and managing stress. And I wondered whether those simple messages would turn out to be a theme of the conference.
While I haven't been able to attend enough of the hundreds of sessions run this week to say for sure, the first lecture I saw on Monday morning certainly continued the pattern. Nobel Laureate Elizabeth Blackburn's talk on the relationship of telomeres and telomerase to stress and disease was a fine example of cutting-edge science enriching our understanding of something that people seem to have known all along--in this case, that stress can age you.
Telomeres, in case you don't know, are areas of genetic material at the end of each chromosome. (Humans and animals have them; so do plants and even pond scum.) The material doesn't code for anything; i.e. it is not genes as such. Instead, telomeres seem to protect the gene-encoding portions of the chromosomes from damage. Telomeres have often been likened to the hard plastic coating on the end of a shoelace, that prevents the lace from fraying.
As cells divide, their telomeres become shorter and shorter. Unless they are repaired by an enzyme called telomerase (which Dr. Blackburn co-discovered in 1984), they will eventually disappear altogether, a situation that wreaks havoc on a cell's DNA and eventually leads to the cell's death.
The length of the telomeres in an individual human's white blood cells can be measured with a simple blood draw. Dr. Blackburn explained that the length of a person's white blood cell telomeres isn't static; it can go up over time, as well as down.
So here's the exciting part: many of the common diseases of aging, Dr. Blackburn said, like arthritis, diabetes, and cardiovascular disease, have been linked to shorter telomeres in normal cells. Short baseline telomere length in a person's white blood cells predicted cancer, heart attack, vascular dementia, and stroke--it even raised the risk of dying from any cause.
Which might not be all that interesting unless there were some evidence that telomere length can change, in ways that we may have some control over. People who increased the level of omega-3 fatty acids in their systems showed less telomere shortening. Avoiding stress may also help. Chronic psychological stress (Dr. Blackburn gave the example of mothers caring for chronically ill children) is associated with shorter telomeres. So are other psychological factors like perceived stress, pessimism, "cynical hostility," major depression, exposure to childhood trauma, past domestic abuse, and so on.
Even better--since how much stress life dishes up isn't entirely up to us--physical activity seemed to mitigate stress-related telomere shortening. The more minutes of average daily physical activity test subjects racked up in a day, the more they were able to erase the effects of stress on their telomeres.
Good sleep quality was related to longer telomeres. And participants in an intensive, three-month meditation retreat came back not only with decreased scores for neuroticism, but with longer telomeres too.
As you might expect, there are some who think that telomerase-based treatments for aging are on the horizon. Whether that's true or not (and it won't be simple, as excessive telomerase activity isn't necessarily a good thing, either), bodies of work like Blackburn's lend concreteness to some of the most ancient ideas about how to live long and well.
The rest of the day
In the afternoon, I attended a session on perinatal mental health, which took on the question of women, pregnancy, and psychiatric medications--a huge and fascinating topic that I'm going to wade into another time.
I also went to a scheduled press briefing, where eight researchers hand-picked by the APA presented their work to a roomful of journalists. Quite a bit of this work was of the common-sensical variety: Cyber-bullying increases suicidal thoughts and plans in teens, especially when combined with school bullying! Cognitive-behavioral therapy delivered by email to immigrants, in their language of choice, was more helpful than no therapy! Childhood neglect makes adults less able to sustain intimate relationships! Etc. I shouldn't be snarky. This is all fine work, aimed at real plights. But by this point in the meeting, I was feeling hungry to discover something really exciting and new, some Next Big Thing, and I was beginning to feel that I was being let down. (Obviously, the Next Big Thing right now is the DSM-5. Yet I hadn't really heard anybody talking about it. It almost seemed as though the organization was exhausted and maybe even a little traumatized by the whole process of writing and publishing the new DSM, and not really in the mood to gloat or be proud. At least that's what I have begun to imagine.)
One surprising thing from the press briefing, which I heard it come up one or two other times over the week as well: There's evidence that a single injection of ketamine (a.k.a. "Special K," a horse tranquilizer and a human drug of abuse) can significantly diminish depression within just 24 hours, in up to two-thirds of people with stubborn treatment-resistant depression. The researcher, James Murrough of Mt. Sinai in New York, said that the treatment isn't ready to go clinical yet. Nor did he say whether the patients are rendered catatonic by the treatment (though he did hint that the amounts of ketamine involved are much less than what recreational users might consume). For my part, I'm glad if psychiatrists are again feeling that it's safe to research the potential of psychedelic substances (ketamine is closely related to PCP)--a fascinating avenue that the excesses of Timothy Leary et. al. gave a bad name to back in the '60s and '70s.