Bench and couch: genetics and psychiatry

Vaughn at Mind Hacks has a nice piece on recent research, reported in Nature, on psychiatric genetics: Mental illness: in with the intron crowd. The original article, Psychiatric genetics: The brains of the family, appeared in Nature on 10 July (but it’s behind a subscription wall if you want to see the original — sorry). Daniel linked to Vaughn’s article in the last Wednesday Round Up (#20), but I wanted to make a further brief comment. Vaughn does a really nice job of laying out the key issues, so I’d recommend jumping over there if this brief discussion whets your appetite.

The problem for neuropsychiatry is that genetic links to psychiatric disorders are proving difficult to clearly define. Abbott explains the situation really well:

Finding genes involved in psychiatric conditions is proving to be particularly intractable because it is still unclear whether the various diagnoses are actually separate diseases with distinct underlying genetics or whether… they will dissolve under the genetic spotlight into one biological continuum. Indeed, some researchers suggest that it would be better to abandon conventional clinical definitions and focus instead on ‘intermediate phenotypes’, quantifiable characteristics such as brain structure, wiring and function that are midway between the risk genes involved and the psychopathology displayed.

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Relax your genes

Image from Good Karma Flags
Image from Good Karma Flags
Relax — it can affect your genes.

A recent article on PLoS One by a research team from the Benson-Henry Institute for Mind/Body Medicine at Massachusetts General Hospital (MGH) and the Genomics Center at Beth Israel Deaconess Medical Center (BIDMC) discusses the genetic effects of the relaxation response, a widespread bodily state induced by different mind-body techniques (such as meditation).

The original piece, Genomic Counter-Stress Changes Induced by the Relaxation Response, was published at PLoS One, and the findings are also discussed on ScienceDaily, Relaxation Response Can Influence Expression Of Stress-related Genes. It’s starting to be a bit of a refrain from genetics research, but it still bears repeating: the team is exploring a way that ‘changing the activity of the mind can alter the way basic genetic instructions are implemented,’ as Dr. Herbert Benson explained (in ScienceDaily).

The relaxation response is a bodily state, found in a variety of contexts, characterized by ‘decreased oxygen consumption, increased exhaled nitric oxide, and reduced psychological distress.’ Long-term effects of relaxation exercises include decreased oxygen intake and carbon dioxide elimination; reductions in blood pressure, heart and respiration rate; prominent low frequency heart rate oscillations; and some changes in cortical and subcortical brain regions, including increased thickness of the cortex (see NeuroReport and here also on the effect of meditation on aging).

For about three decades, dependable clinical studies have shown that relaxation response-producing exercises have a range of positive health benefits. What makes the current research distinctive (at least in my reading) is that the team traced this metabolic process to its genetic effects. As the authors write:

This study provides the first compelling evidence that the RR elicits specific gene expression changes in short-term and long-term practitioners. Our results suggest consistent and constitutive changes in gene expression resulting from RR may relate to long term physiological effects. Our study may stimulate new investigations into applying transcriptional profiling for accurately measuring RR and stress related responses in multiple disease settings.

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Live healthy, turn on your genes

For all those out there who still think that ‘it’s all in the genes,’ here’s a recent news story on the way that changes in lifestyle can affect genetic activity. Will Dunham at ABC News brings us, Healthy Lifestyle Triggers Genetic Changes: Study (I also pulled it off the Reuters feed). The study was small, and I doubt that it was nearly as rigorous as really necessary, but the findings are interesting.

In a small study, the researchers tracked 30 men with low-risk prostate cancer who decided against conventional medical treatment such as surgery and radiation or hormone therapy.

The men underwent three months of major lifestyle changes, including eating a diet rich in fruits, vegetables, whole grains, legumes and soy products, moderate exercise such as walking for half an hour a day, and an hour of daily stress management methods such as meditation.

As expected, they lost weight, lowered their blood pressure and saw other health improvements. But the researchers found more profound changes when they compared prostate biopsies taken before and after the lifestyle changes.

After the three months, the men had changes in activity in about 500 genes — including 48 that were turned on and 453 genes that were turned off.

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Genomics and ‘Post-Neo-Darwinism’

Blogging on Peer-Reviewed ResearchI’ve been trying to put together my reader for a new unit (class) on human evolution at Macquarie University that I’ll be doing next semester. As usual, I’m doing this at the 11th hour, but this should be my last completely new, never-before-taught-at-my-university class for at least a year (I hope). In the process of checking out the most recent edition of my favorite human evolution journals, I happened across an odd and really thoughtful piece by Prof. Kenneth Weiss, who’s at Penn State. In the past, I’ve remarked about ‘post-neo-Darwinism,’ a term that I’m sure causes grimaces and eye-rolling, but that I think is worth discussing (I can’t take credit for the term; I think I heard it from Prof. Emily Schultz of St. Cloud State University at the last meeting of the American Anthropology Association).

By the way, Daniel posted a great ‘Evolution Round Up’ just recently with a whole lot of interesting material (I especially enjoyed Mo’s piece at Neurophilosophy on ‘Synapse proteomics & brain evolution’). We’re not really an evolution theme website, but it’s obvious how important it is to locate brain development in frameworks consistent with evolution. (I’ll come back to why being overly persuaded by evolutionary frameworks can be pernicious in a second, and it’s broader than my recent rant about memetics.)

Unfortunately, because the Weiss piece is more of an essay, in his recurring column entitled ‘Crotchets & Quiddities,’ there’s really no abstract of it, so I can’t link through to a nice concise summary of the piece. So, more than usual, I’m going to copy blocks of text from his essay, ‘All Roads Lead to… Everywhere?: Is the genetic basis of interesting traits so complex that it loses much of its traditional evolutionary meaning?’, before I get into my own commentary. Obviously, if you have access through a good research library, you should be able to get your hands on the original article. (More on Weiss’s columns can be found here — they’re quite good.)

The set-up for Weiss’s discussion is the idea that it doesn’t make sense to talk about ‘THE road’ to any particular place in a complex systems of highways and secondary roads because there are many routes:

With such choices, it doesn’t make much sense to ask, ‘‘What is the road to Rome?’’ In a somewhat similar way, rapidly growing knowledge about the nature of genomes and what they do suggests that what’s good for the Romans is good for biology as well. Instead of a gene for this and a gene for that, we face the possibility that all genes lead to everywhere, which may have important
implications with regard to our understanding of the genetic basis or evolution of traits like the shape of the skull, a skull, or this skull. If all real roads lead to the Circus Maximus, do all our craniofacial genetic roads lead to the foramen magnum?

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The Genetic and Environmental Bases of Addiction

As Presented By: Reid, Takashi, Sheeva and Michael

A man with deep set eyes and a tired, drawn face wanders aisle to aisle, seemingly lost amongst the labyrinth of supermarket shelves. His bloodshot eyes, bent forward posture and slight stature are indicative of years of hard living. His pain is readily apparent as he nervously shifts his weight from one foot, to the other and then back again. He rolls up his sleeve to scratch an unseen itch, briefly revealing a patchwork of new and old needle marks along the veins of his forearms; intermeshed with a few cigarette burns and dry, yellowing skin. How did he get this way you might ask? What is it about this particular man that caused him to become an addict?

The Genetic Element

Today many people would say “his genes” predisposed him to become an addict. Addiction has historically been known as a disease that runs in families, and in the past 30 or 40 years, this long-standing belief has been verified using systematic scientific investigation. The bulk of the research suggests that drug dependence functions much like other diseases, with certain people having a genetic makeup that increases their risk.

This was the case for Caroline Knapp, an alcoholic who skillfully describes her battle and eventual victory over addiction in her book Drinking: A Love Story. Knapp struggles with her genetic predisposition saying, “It’s encoded in my DNA, embedded in my history, the product of some wild familial aberration.” This conclusion is not limited to Knapp. One study found that children of alcoholics were four times more likely to become alcoholics themselves.

Modern scientific inquiries tell us that the inheritance of these addictive tendencies cannot be attributed to a single gene, as is the case for some diseases. Its transmittance is much more complicated.

For instance, genes involved in the metabolism of alcohol can be implicated in increased risk of addiction. For instance a major study found that young men who required more alcohol to experience an effect had higher rates of alcohol problems later in life. However, other genes, including those known to affect behavior and mood, are thought to be connected with addiction as well (National Institute on Alcohol Abuse and Addiction). Currently, scientists point to differences in clusters of genes on chromosomes 1, 2, 3, 4, 7, 11, 15, and 16 as important in chemical dependence (Goldman Review).

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