Conditioned for a tragedy

by Charlotte Gutfreund

Heroin by JohnnyCashsAshes

K.J., a young heroin user died from an overdose of heroin. He had been hospitalized numerous times for his continued drug abuse, so had had his blood morphine levels (heroin is broken down to morphine once in the bloodstream) recorded numerous times. Interestingly, his blood morphine levels were no higher than they ordinarily were, yet this particular heroin injection proved fatal (Gerevich, Bacskai, Farkas, & Danics., 2005). So what was it that made this high tragically different than his previous ones?

K.J. had not been using heroin as steadily recently, due to his frequent hospital visits, but studies have shown that, although tolerance to heroin definitely increases over continued usage, periods of abstinence do not then, re-lower tolerance (Druid, et. al., 2007), so that could not have been the cause of his different reaction this time. The only thing that was different about the last time he injected himself with heroin was that he was doing so in a different location than he normally did (Gerevich, et. al., 2005).

Surprisingly, this is actually in agreement with a phenomenon shown in other studies. In 1985, Siegel and his colleagues gave two groups of rats continued morphine injections of progressively higher dosage. Each time the injection was given in the same location. The highest location was then given again, and half of the rats were in a new location for this last dose. The rats in the new location repeatedly showed a significantly higher mortality rate, even though they were getting the same exact dose as the other group and the same dose as they had been injected with (and survived) previously. This is because, as a conditioned response to the stimuli present during previous drug use, the body learns to “expect” the drug coming when in the presence of these stimuli, and physiologically prepares itself to “tolerate” the drug (Siegel, et. al., 1985). Tolerance for a drug is caused when long-term use of the drug alters the function of neurons in the brain. For example, with long-term use of opiates, brain neurons begin to require higher and higher levels of the opiate in order to function properly. When frequently exposed to a drug, the brain will alter itself to compensate for the effects of the drug, thereby creating a “tolerance”. An increased tolerance means that the person must use a higher level of the drug to get the same effect, and so their tolerance continually increases (Somers, 2006).

The deadliest drug

By Danielle Nedivi

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) .

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.

Models of Schizophrenia

By Alex Herman

crazy mouse moon by indi the thirstyfish

LSD and other psychoactive drugs such as ketamine, psilocybin, DMT, and peyote (mescaline) have for many years held the interest of researchers and scientists throughout the world due to the striking effects that they have on the brain functions and behavior of many mammals.  Psychiatric research in particular was initially drawn to the use of LSD (Lysergic acid diethylamide) as a drug that could produce model schizophrenia in test subjects and patients.  There is a long history of psychedelics research correlated with schizophrenia ever since LSD and its counterparts proliferated in use during the 1960′s and 70′s (Snyder et al. 1974).  In the mid 70′s, certain research conducted by Bowers and Freedman highlighted surprising similarities between the states of some early schizophrenic patients and the effects of psychedelic drugs (Snyder et al. 1974).  Apparently, it was in the acute schizophrenic breakdowns of new patients that the researchers observed effects such as transcendence to new modes of perception and creativity.  Also observed were experiences of both intense dread and elation, attitudes that are frequently alternated between in patients experiencing a psychedelic ‘trip’.

The relationships between psychedelics and schizophrenia are still being explored in today’s research, but now researchers are focusing in on the use of psychedelics as a model to test possible treatments for this debilitating mental disease.  In early studies regarding neurotransmitters and schizophrenia, it was believed to be the abnormal levels and fluctuations of the neurotransmitters serotonin and dopamine that were primarily responsible for the diseases’ dramatic effects, but recent research on mice is uncovering a different culprit acting in the synapses of test subjects: the neurotransmitter glutamate.  The so-called serotonin-glutamate complexes are under intense study made possible by the dosing of lab mice with nominal amounts of LSD and ketamine.  Recent studies done by Stuart Sealfon and other researchers at the Mount Sinai School of Medicine in New York indicate that mice, when dosed with LSD, will experience behavior closely associated with schizophrenia in humans, due to uncontrolled regulation of serotonin receptors in neurons.  These behaviors, however, are canceled out when a drug altering the glutamate receptors is given to the mice, indicating that glutamate transport and reception plays a much more important role in schizophrenia than we had originally thought.

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?

References

University of Delaware Office of Public Relations (1997). Sensational study: Psychology prof’s work ranks among world’s best. Retrieved October 6, 2008, from
http://www.udel.edu/PR/UpDate/97/19/27.html

Author Unknown. (1998, September 9). Sex and the White House. BBC News.  Retrieved October 4, 2008, from
http://news.bbc.co.uk/2/hi/events/clinton_under_fire/the_big_picture/167068.stm

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

http://psychologytoday.com/articles/pto-20001101-000035.html

Carmichael, M. (2008, 12 March). His Cheating Brain. Newsweek. Retrieved October  2, 2008, from 
http://www.newsweek.com/id/121492/output/print

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

Can food be an addiction?

by Rachel Harris

Many addictive drugs, such as nicotine, alcohol, and amphetamines, change the levels of dopamine in an area of the midbrain called the substantia nigra. In disrupting the dopamine systems in the brains, these drugs interrupt the brain’s quest for rewards and control of decisions. Recently, the obesity epidemic has catalyzed many psychologists to examine how food consumption acts on the brain in ways similar to substances more typically associated with addiction. Researchers at the National Institute on Drug Abuse have compared brain images of obese people and methamphetamine users. They have found that fewer dopamine receptors in both groups, when compared to a normal control group. Moreover, the signs of drug addiction‹: developing tolerance, withdrawal symptoms, and overwhelming involvement‹ are also seen with food. [Editor's note: More on food "addiction" in this post on the hazards of delicious food. ] In addition, the absence of food is seen to cause withdrawal symptoms in rats. Although these results cannot be directly applied to humans, this study suggests that food might create powerful motivations to eat not only because the taste is rewarding, but also because eating reduces anxiety or stress.

Death by Meth

by Isabel Vondermuhll

Crystal meth is methamphetamine hydrochloride, the street form of the drug methamphetamine that comes in clear, chunky crystals and is heated and smoked. It is commonly known as crystal, ice and tina.

As for the science behind it, methamphetamine is a chemical stimulant which is similar to amphetamine, but creates a much stronger effect on the central nervous system.  In its legal form, it can be used to treat ADD, narcolepsy and, for short periods of time, obesity.   Mostly, however, it is used illegally for recreational purposes, for weight loss, and to maintain alertness, focus, motivation, and mental clarity for extended periods of time.  Methamphetamine releases high levels of dopamine in the brain, a neurotransmitter that is associated with pleasurable or rewarding experiences.   Meth users tend to display OCD behavior such as obsessive and repeated cleaning.  In withdrawal,  meth users show depression-like symptoms, excessive sleeping and eating, anxiety, and drug craving.

What made me decide to write about Crystal Meth was an acquaintance of mine who has since passed away as a result of his substance abuse.  When I was in high school I interviewed him about crystal meth for a health class presentation.  Click “more” to read some snippets:

Refining the genetics of alcoholism

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.

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.

Reference

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

ADHD, smoking, and bupropion

What constitutes the main effect of a drug, and what constitutes the side effect?  Aspirin relieves headaches, but also thins your blood as a side effect.  Unless you are taking aspirin to prevent a heart attack, and then it is the other way around.  With psychoactive drugs, that target one or more neurotransmitters, it can be even harder to sort out.  It takes complicated research to figure out the complicated effects of many psychoactive medications.

Here is a story about a complicated study that looks at one effect of one well-known drug, bupropion, which is marketed as both Zyban and as Wellbutrin. The patients studied were all ADHD patients, boys and girls, ranging from 9 to 18 years old. Half were given a daily dose of bupropion, and half were given a placebo, and then they were followed for about a year.

Wellbutrin is marketed as an antidepressant. Why give people with ADHD an antidepressant? At first glance, this seems odd at best. Most modern antidepressants, like Prozac, Paxil, and Zoloft are SSRIs (selective serotonin reuptake inhibitors). They primarily target the neurotransmitter serotonin, which helps to regulate mood, among many other functions. Wellbutrin, by contrast, targets dopamine primarily, as well as norepinephrine and serotonin. All three play a role in mood regulation, so Wellbutrin provides an alternative when SSRIs are not very effective. Norepinephrine and serotonin may be at least as important in depression, but it is the dopamine that we focus on here.

Dopamine is another neurotransmitter, one that is associated with motivation, pleasure, rewards, and addiction. Ritalin, the best-known drug which is used to treat ADHD, boosts dopamine levels. According to Nora Volkow, of Brookhaven Laboratories,

“We now know that by increasing the levels of extracellular dopamine, you can activate these motivational circuits and make the tasks that children are performing seem much more exciting. By raising that level of interest, you can significantly increase the ability of the child to focus on the task.”

In other words, a controlled rise in dopamine levels improves motivation and focus in kids who have trouble with both.

Compared to cocaine or amphetamines, which also boost dopamine, ritalin’s action is much slower (when taken in pill form). That probably explains why cocaine and amphetamines are highly addictive, but Ritalin is not. A slow boost in dopamine may also explain why bupropian/Wellbutrin is effective as an ADHD treatment. It is working in a similar fashion to Ritalin, though by a different chemical mechanism.

So one drug, bupropion, is useful in treating both depression and ADHD. But what does this have to do with smoking?

Zyban, which is exactly the same drug as Wellbutrin, is marketed as a helper in stopping smoking. As far as I know, there is no definitive research to show how it works. But I will speculate that since nicotine in cigarette smoke provides a dopamine boost, nicotine withdrawal involves the body expecting that dopamine boost and not getting it. Zyban may relieve that craving by raising dopamine levels, although more slowly and not as much as nicotine does.

Now, back to the complicated study. If bupropion (as Zyban) helps people quit smoking, should it also help adolescents avoid smoking in the first place? Dr. Michael C. Monuteaux and his colleagues (reported in the Journal of Clinical Psychiatry, July 2007) tested this by experimentally manipulating whether patients got bupropion or a placebo. They could not, of course, manipulate whether the patients had ADHD. They all did. Nor did they control whether they were taking Ritalin or another stimulant-based drug, but they carefully tracked this. They had patients of different ages, but the results cited in the news story do not point to any age-related differences. They checked on the outcome variable, whether or not the patients smoked, by looking for a nicotine by-product in their urine.

The result must have been disappointing: The patients in the bupropion group were actually more likely to start smoking than the patients in the placebo group.  The drug that works well for stopping smoking was no good at all in preventing these patients from starting to smoke.  I don’t know why that was any more than Dr. Monuteaux.  I can speculate that maybe starting and stopping reflect different underlying neural mechanisms.

There was another result.  Unexpectedly, the patients who were taking stimulant-based drugs, like Ritalin or a generic equivalent, were less likely to smoke.  So now Ritalin may turn out to have an unexpected, but beneficial side-effect.  As usual, we need more research.

One question lingers with me most of all: Why are kids with an ADHD diagnosis more likely to take up smoking in the first place. Some researchers have suggested that this is an attempt to self-medicate. That raises the interesting possibility that understanding more about nicotine addiction may help us to understand more about ADHD as well. But I promise it will still  be complicated.

Just another teenage overdose?

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.