Psychology in the News

May 23, 2009

The deadliest drug

By Danielle Nedivi

China by babasteve

China by babasteve

It’s a question that we have all wondered about at some point. No matter if we are active users, casual dabblers, or outside observers- the mystery confounds in all contexts: why do people smoke cigarettes? Today, virtually everyone in the United States knows that smoking is bad. School programs, public service ads, flyers, doctors- even the cigarette boxes themselves- have drilled that into our brains incessantly enough. Yellow teeth, wrinkles, short breath, not to mention heart disease, lung disease, cancer- the list is seemingly endless. And yet, despite all of the well-known detrimental consequences, smoking is still very much a prevalent activity throughout the US, with the young generations just as much as the old.

According to the American Cancer Society, more than 3,500 people younger than 18 try their first cigarette every single day, and 1,100 others become regular daily smokers. About one-third of these kids will later die from a smoking-related disease. Considering that we all know about this deadly effect, why try that fateful first cigarette in the first place? The answers vary from person to person, but overall they tend to cover the same ground. Some studies have shown social influences from peers to be a major cause. Powell (2005) showed that moving a high-school student from a school where no children smoked to a school where one quarter of the youths smoked would increase the probability that he or she smoked by about 14.5%. Overall, based on 2007 data from the Centers for Disease Control (CDC), 20% of high school students smoke. Many prefer not to feel left out or appear antisocial by not taking risks or trying new things, and they are willing to compromise their health to achieve that crucial sense of belonging. The health-deteriorating factor of cigarettes is too elusive and vaguely far off to feel critical- if anything, their immediate effects are mostly positive.

Smoking provides many enticements on top of its well-advertised drawbacks.  Cigarettes stimulate receptor sites for the neurotransmitter acetylcholine, and provide a short term boost in dopamine levels.  The results can be a  temporary yet immediate calm and solace to a smoker . They can also render potentially awkward moments such as breaks from conversation natural (Dichter, 1947). They provide a smoky, mature voice and a feeling of sophistication and nonchalance. That society has brought many to believe that smoking is “cool” does not help matters. In media from films to books to songs, from GQ photo spreads to “Breakfast at Tiffany’s,” the smoker is usually presented as an alluring rebel worth striving to imitate. “Chain smoking” and “clove cigarettes” have become unpredictably glorified terms. At least at the moment, the image of the slightly neurotic, jaded, risk-taking smoker is trendy, and people will go far to emulate it. Even in college, where we believe students are not only more intelligent and mature but also less impressionable, cigarettes still appear all over the place and incite a mystique the influence of which is difficult to shake off, even for those who had successfully avoided the offender thus far (Reed, 2006) . (more…)

May 12, 2009

Love, obsession, and chemistry

by Dan Schwarzman

May 22nd (Dont Say That You Love Me) by Phoney Nickle

May 22nd (Don't Say That You Love Me) by Phoney Nickle

What is love, and why does it exist? Chemical similarities have been found linking love to OCD and depression. Anthropologist Helen Fisher PhD of Rutgers University has been doing research on love, which she has divided into three chemically separate states. Fisher says that lust is driven by androgens and estrogen, while romantic love, characterized by intensely emotional mood swings and obsessive craving, is driven by high dopamine and norepinephrine levels, along with low serotonin. The third state, of stable attachment, is driven by the hormones oxytocin and vasopressin.

An evolutionary anthropologist, Fisher explains the evolutionary value of these three states. According to evolutionary theory, adaptations show up in species if they lead to increased survival and reproduction. Fisher says that lust evolved as a mechanism for people to be interested on a basic level in reproduction with others, while romantic love developed to focus one’s mating energy on just one individual. Stable attachment works to tolerate this individual long enough to raise children as a team. The obsessive energy output of being in love might seem illogical in the context of evolutionary theory, especially since love is often not reciprocated, but this ability to forgo short term efficiency in favor of greater long term reproductive success makes sense as an important adaptation for the continuation of the human race. (more…)

November 5, 2008

Seeking sensation through sex and politics

by Molly Tulipan

Bill Clinton and Monica Lewinsky. Warren Harding and Nan Britton. JFK and Marilyn Monroe. Sexual scandal has permeated the White House since America can remember.  Why do leading politicians risk their national reputations and their jobs for extramarital sex? The answer might just lie in their chemical makeup.
Monoamine oxidase A (MOA) is an enzyme that helps our bodies regulate important neurotransmitters like Dopamine. Involved in emotion, learning, and attention, this chemical messenger also has numerous links to risk-taking (Myers, 2006). Zuckerman (2000) discovered that people with sensation-seeking personalities often have excessive levels of Dopamine activity.  This is where MOA comes in to play; people who take fewer risks have higher levels of MOA, because MOA regulates Dopamine. Most people have enough MOA to keep their risk-taking behavior under control. For instance, older people have more MOA than younger people and thereby exhibit less frequent risk-taking behavior. (Ever wondered why young adults are more likely to put themselves in sticky situations than their grandparents?) Females have more MOA than males and are less likely to put themselves in dangerous situations such as drinking and driving and excessive drug use.  What happens when you don’t have sufficient MOA? Essentially, lower levels of MOA yield more dangerous behavior.

In 1971, psychologist Marvin Zuckerman linked levels of MOA to another behavior: sensation seeking, a term he coined.  Zuckerman created a complex personality test called the Sensation-Seeking Scale. Sensation seekers are characterized by a tendency to put themselves in new, exhilarating situations even if they are dangerous. People that pass for sensation seekers as defined by Zuckerman are also easily bored, particularly by repetition in the workplace, “predictable” experiences with others, and conventional work assignments (Zuckerman, 1964, cited in The University of Delaware 1997). It comes as little surprise, then, that sensation seekers might crave the excitement and volatile environment of the White House, and similarly, that their thrill-seeking personalities might also lead them to reckless sexual behavior.

MOA is not the only explanation for sensation seeking. As is always the case with assessing personality traits, risk-taking personalities are a delicate combination of nature and nurture. However, it is interesting to consider that the same traits that lead someone to such a high position of power might also lead them down the risky path of adultery. Even more fascinating: are these traits linked to chemicals in our bodies that lie partly beyond our control?


University of Delaware Office of Public Relations (1997). Sensational study: Psychology prof’s work ranks among world’s best. Retrieved October 6, 2008, from

Author Unknown. (1998, September 9). Sex and the White House. BBC News.  Retrieved October 4, 2008, from

Zuckerman, M. (2000, November) Are you a Risk Taker? Psychology Today.  Retrieved October 4, 2008, from

Carmichael, M. (2008, 12 March). His Cheating Brain. Newsweek. Retrieved October  2, 2008, from

Myers, D. (2006). Psychology (8th Edition in Modules). New York: Worth Publishers.

March 14, 2008

To sleep, perchance to be temporarily paralyzed…

Filed under: neurotransmitters, sleep — Tags: — intro2psych @ 4:12 pm

by Suzanne Rozier

One night last summer, I experienced waking up several times from deep sleep to find that I couldn’t move any part of my body (except for my eyes). Feeling that there was some other presence in the room lurking at the foot of my bed, I tried over and over again to turn my head so I could see what was there; once I could finally move again, I found that there was nothing.

In the morning, fully awake, I realized that what I had experienced the previous night was a mild episode of sleep paralysis, something I had read about before on the Internet. Sleep paralysis is a brief state of being unable to move ones body upon either falling asleep or waking up, and it’s usually accompanied by an ominous feeling that there is some kind of ghost or demon in the room, or even visual or auditory hallucinations.

J. Allan Cheyne of the University of Waterloo has conducted a significant amount of research related to sleep paralysis, and has compiled a comprehensive website ( detailing the results of his research, as well as a survey to fill out if you have ever experienced this phenomenon. According to his research, first episodes of sleep paralysis typically occur to adolescents, suggesting it as a possible reason for children’s fear during the night. Sleep paralysis has also been associated with narcolepsy, although not all narcoleptics experience it and not all people who have experienced sleep paralysis have narcolepsy.

The biological explanation for sleep paralysis is simple: when we are asleep, certain neurotransmitters are blocked out in our brain to prevent us from acting out our dreams. Sleep paralysis occurs for the few moments either immediately before we go to sleep or right after we wake up, when we are conscious but those neurotransmitters are still being blocked, preventing us from moving. (

I haven’t experienced sleep paralysis again since that night last summer, and it may never happen to me again. With some people it happens periodically, and some people will never experience it at all. But now you know: if you ever wake up and find yourself paralyzed, don’t freak out — it will go away soon.

December 23, 2007

One good thing about stress

Filed under: brain wiring, health, neurotransmitters — Tags: , — intro2psych @ 3:21 pm

by Max Friedman

We have learned that stress leads to increased glucose levels in the bloodstream, which can increase the amount of plaque in our arteries and result in heart attack or stroke. We have also learned that stress temporarily shuts down white blood cells due to increased cortisol levels in the bloodstream, allowing us to gain a temporary boost of energy. But did you also know that stress can help alleviate pain?

Yes, it’s true. The pain from that scrape on your knee will melt away when a tiger finds its way into your dormroom. An article in Science Daily details a recent study regarding this phenomenon known as analgesia. Researchers from the Queensland Brain Institute in Australia have found the specific mechanism of how noradrenaline, a stress hormone released during the “fight or flight” reaction, interacts with the brain to reduce pain. Their experiments on rats using electrical stimulation revealed that noradrenaline suppresses transmission between synapses on the pathway from the pontine parabrachial to the amygdala by activating adrenoreceptors. It is one small step towards fully understanding the enigmatic workings of the brain.

September 29, 2007

Refining the genetics of alcoholism

Filed under: addiction, dopamine, drugs, neurons, neurotransmitters — intro2psych @ 8:31 am

by Rachel Harris

The idea that alcoholism has a genetic component has gained credibility over recent decades. Previous research has studied the association of the dopamine receptor gene (DRD2) and alcoholism. However, a new study—fixing the limitations of prior research—was recently conducted. Presenting inconsistent findings, this new study claims that a neighboring gene called ankyrin repeat and kinase domain (ANKK1) may also be involved in forming addiction, including alcoholism. Working on a project for the Collaborative Study on the Genetics of Alcoholism (COGA), researchers across the United States conducted the research, which involved marking the dopamine receptor gene and other genes in the surrounding area. Using a sample of Caucasian families, the study found that the ANKK1 gene provides the strongest association to alcoholism. Although the findings of this research are extremely important to the study of genetic influences on alcoholism, they are not conclusive. The study does not prove that ANKK1 is involved in alcoholism any more than DRD2; it only shows that a strong association exists. The results “must be interpreted with caution and further explored.” [1] More studies need to be conducted to verify the results.

beer bottles

Furthermore, when fully exploring the psychology of addiction, it is important to look at the formation of alcoholism as a combination of genetic and social factors. Individuals are shaped both by genes and the environment. Environmental factors, such as the social skills learned from one’s family and other daily social interactions, can influence the development of alcoholism. Moreover, alcohol is a prevalent part of our culture. Forces in American society, such as advertising, can contribute to an individuals’ decision to drink. Thus, it is important to continue to research the origins of disease of alcoholism, as the development of the disease consists of complex factors.


[1] Genetic Influences on Addictions-New Findings. Medical Research News.
25 September 2007.

August 28, 2007

What if Monk were a mouse?

Filed under: genes, neurotransmitters, SSRI — Tags: , — intro2psych @ 4:36 pm

My favorite obsessive compulsive detective, Monk, may never clear up the mystery of who killed his beloved wife, but scientists are closer to clearing up the mystery of why Monk is obsessive compulsive. The new discovery is that mice who are missing a protein called SAPAP3 act like they, too, have OCD (obsessive compulsive disorder). They do not boil their toothbrushes before using them or wash their hands 100 times, of course, but then the compulsive behaviors of humans vary quite a bit from individual to individual anyway. Just like humans, these OCD mice exhibit what looks like an unhealthy obsession with cleanliness. They lick and groom themselves to the point of destroying their fur, and damaging their skin. They do this even when they should be sleeping. They do not solve mysteries, so far as we know.

Adrian Monk

How is it that these mice were missing that particular protein? Well, these are very special mice. They have been genetically engineered. Specifically, the gene that codes for SAPAP3 has been removed, or “knocked-out” of their DNA. We can call them SAPAP3 knock-out mice. And they were created for that best of scientific reasons: the researchers just wanted to see what would happen if you took that gene out.

This story should raise a lot of questions in the minds of readers who do not have a lot of background in genes and behavior.

Q: What does knocking out a gene affect a particular protein?

A: We think of genes as just being a kind of code, that passes on information about traits from parents to children. But in fact, genes are much more than that. They are protein factories. What you inherited from your parents are 23,299 little protein-building machines. It is the proteins they build that do the work of every cell in your body. Different kinds of cells get different proteins, because different genes are switched on and off for different cells. So these SAPAP3 knock-out mice have had the genes for that one protein effectively turned off for every cell.

Q: Why does a protein affect grooming behavior?

A: Like any behavior, grooming involves a great many neurons (nerve cells). Neurons “talk” to each other by means of chemicals called neurotransmitters. One neuron releases a neurotransmitter, and the next one picks it up. SAPAP3 plays a role in the transmission of the neurotransmitter glutamate. What brain circuitry is being messed up by the lack of SAPAP3 is not clear. Since glutamate is an excitatory neurotransmitter used all over the nervous system, there are many possibilities. So we know that the lack of SAPAP3 is interfering with the normal function of the nervous system, but we do not know exactly what it does to increase grooming.

I should also point out that the neurotransmitter more often associated with OCD and other anxiety related disorders is serotonin.

Q: Is there anything that can be done for these poor mice?

A: Yes! As it turns out, they respond to fluoxetine (prozac). This drug, which is also used to treat OCD in humans, significantly reduced their grooming behavior. This drug is a serotonin specific reuptake inhibitor (SSRI),  which only makes the glutamate connection more puzzling.

Q: Is Adrian Monk an SAPAP3 knock-out human?

A: Not in the same way as the mice. He has not been genetically engineered. But it is possible that natural genetic variations among humans contribute to OCD. It is also possible that lower production of this protein is involved in OCD in humans, but we will need new studies to look at this.

Something to keep in mind whenever you read a story about a gene that has been identified with this or that disorder: Just because the gene plays a role in some individuals does not mean that the same gene plays the same role in everyone. There might be multiple genes involved. There might be many pathways to the same illness. In fact, it is an entirely different gene linked to OCD that most researchers have been focused on the past several years.

One thing is clearly different between mice and men (at least OCD mice and men): For these mice this is purely genetic. In humans, it may be a mix of genes and experience. In some humans, that experience may be a strep throat, which then triggers an autoimmune response. Family dynamics and life stress certainly play a role in the ups and downs of OCD, but probably not in creating it.

Finally, it is worth pointing out that the mice’s behavior might not really be analogous to OCD in humans. OCD is one kind of anxiety disorder, but not the only kind. Self-grooming is a way to calm anxiety. Then again, so is touching every parking meter on the sidewalk as you go by, if you are Adrian Monk.

August 27, 2007

Why exercise should be part of your study regimen

Filed under: development, drugs, neurotransmitters — Tags: , , — intro2psych @ 10:26 pm

We all know exercise is good for our bodies. And yes, our brain is a part of our body. But does a good workout at the gym really do anything for our brains? The answer might be yes.

In this NYT science page article, author Gretchen Reynolds makes the connections between exercise, blood flow to the brain, and neurogenesis, the process of adding new neurons to the brain. In a nutshell, the idea is that by exercising you increase blood flow to the brain, which then has more raw materials at its disposal to create new neurons.

Why do you need new neurons? Actually, that isn’t all that clear yet (at least not to me). We know that we are born with plenty of neurons, and most of them stick around our entire lives. But in the last 10 years or so, we have learned a lot about the process of creating new neurons, mostly (or all) in or around the hippocampus.)

hippocampus & amygdala


There is an interesting critique of this article here, in which blogger Jake Young accuses Ms. Reynolds of getting the facts right but the interpretation wrong. He is certainly correct that the Morris Water Maze (MWM) is more of a spatial memory test than a “rat IQ” test. The rest of his argument boils down to this: The science around the hippocampus, neurogenesis, and memory is not nearly as clear as Ms. Reynolds states it. All true. But it is hard to resist the speculation that neurogenesis might have something to do with long term memory, since it does take place around the hippocampus, and the hippocampus is clearly involved in the creation of new long term memories. Perhaps she could have been more clear about what parts of the story were more speculative than others.

August 17, 2007

Just another teenage overdose?

Filed under: addiction, dopamine, drugs, neurotransmitters — intro2psych @ 3:03 pm

British 17 year old Jasmine Wills went to the hospital following an overdose of a drug that is increasingly popular with teens in both America and Europe: Caffeine. Specifically, she drank seven double espressos over the course of her shift working as a waitress in her dad’s sandwich shop. The details can be found in The Guardian.

Poor Jasmine was probably just trying to counter the effects of the neurotransmitter adenosine, which is what makes us drowsy. It would not be a good thing to yawn in front of her dad’s customers, after all. But, like all drugs, caffeine has multiple effects. In this case it was the stimulation of the autonomic nervous system that landed her in the hospital. And the pleasurable effects of caffeine, most likely due to the stimulation of dopamine release, probably also played a role.

I was also interested to see she had developed a powerful aversion to coffee from the incident. As anyone who has ever experienced food poisoning can attest, humans are able to learn to avoid a taste or smell after a single strong negative experience. From now on, she will probably have to stick to tea.

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