The evolution of ADHD

by Eric Schuman

Photo by by Ptit@l

Research has shown that ADHD (Attention deficit / hyperactivity disorder)  is strongly influenced by genes. It seems as if it is related to a problem within the dopamine reward system of the brain. Difficulties with this system could be the  reason that people with ADHD and ADD (attention deficit disorder) seem to have trouble staying focused.

The bad side of  ADHD is pretty obvious: It makes people seem unfocused, hyperactive. But new research proposes that it has benefits. Why else would the genes associated with ADHD still be in the gene pool?  Researchers Dan Eisenberg of Northwestern University and Ben Campbell of the University of Wisconson, Milwakee, think they have an answer. In a study published in BMC Evolutionary Biology, they posit that the sort of activities associated with ADHD—a want of novelty, behavioral flexibility, being hyper-aware in environments—were in fact advantageous to nomadic herdsman. They  go on to link ADHD to obesity. In the modern world where a scarcity of food (for many but clearly not all) no longer exists, dis-inhibition of seeking pleasure from things like food become exaggerated, leading to obesity. Many  children with ADHD have higher BMI’s (body mass index) than their peers, before they go on  medications that often lead to weight loss, they point out.

Campbell, Eisenberg and their collegues (2008) studied a tribe in Kenya. One half had stayed nomadic, and the other had become agricultural. They  explain that within a nomadic context, the ADHD genes are beneficiary. When in a more sedentary context, those same genes result in increased weight and malnutrition. This allele that contains these genes is, of course, connected with ADHD. Therefore, it seems ADHD is both positive and negative.

Newly discovered mutations tied to schizophrenia

by Stacy Locke

Psychologists have long been trying to unravel the mystery of schizophrenia. A recent study has found rare genetic variations in Schizophrenic patients that were previously undetected, which could point us in the right direction to understanding why and how a person develops schizophrenia.
The New York Times Science section reveals the new analysis, originally published in the journal Science. The researchers detected rare and unknown genetic mutations that occur three to four times more often in Schizophrenics than others. This collaboration involved the National Institute of Mental Health, The University of Washington, Seattle, and Cold Spring Harbor Laboratory. Blood samples were analyzed from 150 Schizophrenics and 268 people with no psychiatric disorders, using a new high-resolution technique. 53 of these mutations were found overall, showing not only a tendency in Schizophrenics, but also in a specific sub-group that developed the disorder in childhood. This discovery could point to an even more complex underlying genetic reason for the disorder than was previously believed.
This new study could indicate a new direction in Schizophrenia research, but even the senior author Jonathan Sebat admits that there is a long way to go and the findings could mean very little in the grand scheme of things. The most important thing to be taken from this study is that it provides evidence that the new high-resolution scanning technique can be successfully used to find minor genetic variations. “The take-home message is that there’s a new way to search for genetic links, and this new method goes straight to the underlying biology,” stated Sebat. This means it could help with understanding many disorders, not just schizophrenia.

Reference:

Carey, B. (2006, March 25). Study Ties Genetic Variations to Schizophrenia. New York Times.

http://www.nytimes.com/2008/03/28/science/28gene.html?_r=1&oref=slogin

A Valentine’s Day Mystery

by Stacy Locke

Love is one of the greatest mysteries of life: How does one individual become attracted to another? And furthermore, can the potential for, and longevity of, a relationship be predicted?

The February 2008 issue of Psychology Today lends some new insight into love within the article “Scents and Sensibility.” The article describes new research that connects attraction and compatibility with scent. A biologist at the University of Lausanna in Switzerland, Claus Wedekind, conducted a study that lends great evidence to this theory. 44 men were given new, clean t-shirts and asked to wear them for two nights straight without using any extraneous, artificial scents. 49 women sniffed the shirts and specified which odors they found most attractive. Results showed a strong tendency for women to prefer the scents of men who were “immunologically dissimilar to them,” that is, men who differ in their genetic code in terms of MHC or major histocompatibility complex, which helps the immune system recognize pathogens. This would serve a biological purpose in that it creates couples that will produce more disease-resistant children.

Interestingly enough, however, a similar study conducted by Martha McClintock found that women were not attracted to the scent of men who had none of the same MHC genes as them. This suggests that there is a critical balance point between too much in common and too much difference. Geneticist Carl Ober found that couples with high MHC similarity had more trouble conceiving. Furthermore, Psychologist Christine Garver-Apgar found a correlation between high MHC similarity and a high likelihood of cheating.

Could these findings prove once and for all the existence of “sexual chemistry?” Should we all go without perfumes and scented products so as to not distract from our natural scent? Perhaps love can be explained in a psychological context much more easily than we ever thought.

Reference:

Svoboda, E. (2008). Scents and Sensibility. Psychology Today. 41(1), 66-73.

Do-gooder genes?

by Kenia Rodriguez

As a native New Yorker I am used to watching dozens of people walk right past donation tables or street beggars without even a second thought. I’m actually surprised when people do take the time to stop and give a quarter or a nickel. But what it is about these particular individuals that makes them more likely to give money to others?

Dr. Ariel Knafo of the Psychology Department at the Hebrew University of Jerusalem and his team have been wondering just that. In a recent study, subjects were to play an online game and in which they would be awarded $12 for their win. The players could either choose to keep the money or give part or all of it to an anonymous other player. Samples of DNA from each subject were also taken prior to the experiment.

The results of the experiment were quite surprising. Those subjects who had variants of a gene called AVPR1a gave, on average, about 50 percent more money than those who did not display the gene variant. The gene AVPR1a codes for the activation of the hormone Vasopressin which is responsible for social bonding. This means that a relationship exists between genetics and human altruism.

But how quick are we to believe that human generosity is owed to genetics? The results of this experiment bring about an interesting clash between the social teachings on morality versus the biological attributes of behavior. If our generosity is genetically based and has therefore served some evolutionary purpose (possibly to encourage cooperation between social groups to improve changes of survival), then why does it appear that generosity is so hard to find?

Suicidal thoughts, SSRIs, and genes

by Kelly Long

In a world where illnesses once thought debilitating have become more treatable than ever, the question of whether or not a treatment is available for an affliction like depression has become almost obsolete. The difficulty has shifted to the issue of which drug is best for which patient, and how a balance may be found between treatment and side effects.
Recent government-funded studies, reported in the New York Times, have shown that Celexa, an anti-depressant drug belonging to the class of selective serotonin reuptake inhibitors (SSRIs) may cause patients to experience suicidal thoughts. Interestingly, those same suicidal thoughts tended to be found in patients who did not actually attempt suicide, while it has been noted that the one patient in the study that did actually attempt suicide vehemently denied any thoughts of suicide.

Unsurprisingly, the physiology of the connection may be traced to the brain. Throughout the course of the study, two out of the sixty-eight genetic markers studied were noteworthy, as 36 percent of the subjects in possession of the markers experienced suicidal thoughts after taking Celexa. The markers coded for an amino acid called glutamate, which, aside from working as a natural antidepressant by activating neurons, is involved with learning and memory in the brain. Although the results of the tests were inconclusive, they raise the serious question of how treatment can be achieved without a flurry of undesirable (and sometimes dangerous) side effects. It is also remarkable to think that, with time and more research, a genetic test may be developed that is capable of pinpointing exactly which depression treatment is best for each patient.

[Editor's note: Interested readers may also want to look at this post about why the added caution around SSRIs also causes problems.]

Source:

Carey, Benedict. (2007 September 28). Genes Tied to Bad Reactions to Antidepressant Drug. New York Times. Retrieved September 30, 2007, from http://www.nytimes.com.

Sick and Lonely, a perfect match?

by Sean Boley

A group of scientists at the University of California Los Angeles and
the University of Chicago has recently set out to determine the what
causes the correlation chronically lonely individuals and a high rates
of sickness and death (“Sick? Lonely? Genes tell the tale.”). There are two theories
attempting to explain the reported (House, J. S., Landis, K. R. &
Umberson, D. (1988). Social relationships and health. /Science, /241,
540-545.) correlation between lonely people and rates of sickness. Some
scientists argue that the higher rates are due to a lack of friends and
neighbors to urge the lonely person to see a doctor. Others, the
scientists in the aforementioned study included, think that there is
something intrinsically different in the bodies of lonely people.

By studying the genome of very lonely individuals (volunteers who said
they have not felt close to someone for four years), the researchers
found that a certain subset (about 200) of the 22,000 human genes varied
in this population from normal people. It turned out that many genes in
this subset regulate immune system function, such as the response to
tissue damage and antibody production.

The question that arises is the age old, ‘which came first’ dilemma. Did
the chronic loneliness of the participants lead to a change in the genes
for immunity, or did the lack of certain immune functions cause a change
in the social behavior of the individual. This change in social behavior
could be the cause of either an internal aversion to social contact, or
an aversion by other people to contact the chronically sick person. This
could be a great example of adaptive evolution, as it would be
evolutionarily advantageous to stay away from people who always are
catching infections diseases.

I am of the opinion that any one of these explanations could be playing
a role in the observed correlation. Most likely, they are all playing a
minor role. This certainly presents itself as a promising area of
gene-behavior research. For example, one could study individuals who
have already have depressed immune systems, and observe their level of
loneliness. Alternatively, one could also study the behavior of normal
individuals toward individuals who are chronically sick.

Anecdotally, when I am sick, I don’t really feel like going out and
making friends. Could the explanation to this complex gene-behavior
relationship be as simple as that?