Marijuana, Tobacco and teenage behaviors

by Jenna Rieder

Though marijuana’s popularity has fluctuated over past generations, it remains a major drug used by teenagers and young adults. Marijuana’s “high,” achieved through interaction of the active ingredient, THC, with cannaboid receptors in the amygdala, hippocampus, and areas of the frontal and motor cortices, can affect motor activities as well as cognition and emotion (Myers, 2007). Yet, different studies suggest various amounts of harm posed by the drug, leaving scientists to question the level of danger surrounding marijuana use. One Swedish study found that marijuana users who abstain from tobacco products are generally unaltered. The study tested students from ages 16-20 who reported using marijuana, marijuana and tobacco products, or neither substance. Although nonusers proved more motivated and successful than marijuana and tobacco users, teens who used only marijuana suffered few consequences. The teens smoking only marijuana tended more towards athleticism, good peer relationships, high grades and motivation. Nonusers were ranked similarly in these categories. In general, marijuana users fared well socially, showing no defects in their interactions and relationships. Interestingly, another study echoes these results, though making a distinction between regular and sporadic marijuana users. Researchers tracing emotional intelligence among different groups of teens found that occasional marijuana users exhibited high levels of emotional and social comprehension. Teens who used marijuana more often, on the other hand, exhibited strained interactions and lower understanding.These results are striking, considering marijuana’s long-term effects on different regions of the frontal cortex and limbic system. Given the drugs tendency to linger in the body, affecting skills like cognition for months after, similar affects on emotion would be expected. Perhaps the emotionally instability and confusion associated with marijuana stems from the fact that teens facing these insecurities are more likely to use drugs. Though teens who occasionally use marijuana may exhibit some sense of rebellion and lawlessness, they also practice moderation. This sense of moderation may reflect stability, thus shielding the teens from emotional consequences. However, marijuana may also affect cognition and emotion differently. Interactions of THC with cannaboid receptors in the frontal cortex may differ from those between THC and receptors in the limbic system. Further physiological study of these interactions could be an interesting topic of research.[Editor’s note: It is interesting that the studies in this post are all based on correlational data. As the last paragraph suggests, there is always more than one possible explanation for a correlation.)

Reference:

Myers, D. G. (2007). Psychology. (8th ed.) New York: Worth.

Does smoking cigarettes lead to other drug use?

A report titled Tobacco: The Smoking Gun issued by  National Center on Addiction and Substance Abuse at Columbia University shows that teens who smoke cigarettes are more likely to drink alcohol and smoke marijuana than teens who do not smoke cigarettes.  A press release  and the full report are available from CASA.   The implication, as you might guess from the title, is that tobacco use plays a role in leading teens to use these other drugs.  They support this argument by noting that nicotine use effects the neurotransmitter receptor sites for dopamine and serotonin, two neurotransmitters involved in addiction and mood, respectively.

The numbers and science look pretty impressive, until you start to realize that this is all correlational data.   When asked by Will Dunham of Reuters if smoking  causes teens to abuse other drugs, former health secretary and head of CASA Joseph Califano had to admit “the jury is probably still out.”

Here is why this research does not deliver a clear verdict on cause and effect: A correlation shows a relationship between two variables.  There are always multiple possible cause and effect relationships that could explain the relationship.  An easy way to think about the possibilities is that X could cause Y, Y could cause X, or some other variable, Z could cause X and Y.  In this case, we should wonder, for example, if nicotine causes marijuana use, or is it the other way around.   And given what we know about individual differences in susceptibility to alcoholism and other addictions, we should certainly consider the possibility that these differences make some people more likely to use any and all of the substances they discuss.

There is no question that smoking is addictive and bad for you.  But I’m not sure this report really does anything to further our understanding of the relationship between smoking and using other addictive drugs.  Maybe it will spur somebody on to try a more clever research design.

Binge drinking and social ills: cause and effect?

I suppose people have been saying that alcohol leads to bad things for centuries, even millenia. So new research that links teenage binge drinking with drug abuse, homelessness and imprisonment later in life isn’t exactly news. We do know more than we used to about alcoholism and teenage brains, but a correlation still won’t tell us much about cause and effect.

However, it does make a great thought exercise for students learning about correlations. Since the researchers show a correlational relationship, what are the possible cause and effect relationships that could be involved? As always, you should be thinking about relationships in the form of X causes Y, Y causes X, or Z causes X and Y.

I should note that this is a special kind of correlational study, sometimes called a “forward study.” This means that they measure one variable, and then move forward in time before measuring the other. (You could just as well call it a “before and after” study.) In this case, they measured drinking and particularly binge drinking in the teenage years, and compared that to a variety of measures of adult social functioning more than a decade later. This kind of study pretty much eliminates the Y causes X hypothesis. You cannot argue that homelessness at age 30 caused binge drinking at age 18, for example.

I wrote this when I should have been sleeping

And evidently, I have a lot of company. Americans are skipping sleep to fit everything else into their busy lives, according to Mathias Basner of the University of Pennsylvania. He looked at data collected from nearly 50,000 Americans who were surveyed by the federal government between 2003 and 2005. Here’s what’s bugging me: His conclusion appears to be based on a simple negative correlation between hours of work, and hours of sleep. From this he concludes that working more leads to sleeping less.

So you tell me, students, what are some alternative hypotheses that could explain this correlation?

Meanwhile, a British sleep expert is decrying the “junk sleep” of teenagers. None of you would ever talk on a cell phone or listen to your iPod when you know you should be sleeping, right?

And in Denmark, there is a movement to give night owls the right to sleep late, instead of conforming to an 8-4 culture. Just in case you are wondering, you still have to come to my 9AM class, if that’s the one you enrolled in.

Will my children ever learn to love Szechaun Shrimp or Chicken Molé?

Some of my favorite foods are what American kids call wierd. The sort of food that kids take one fearful look at, and reject out of hand. It is pretty much expected that children will not eat something that looks exotic, smells funny, and is known to be spicy. Not even if I tell them it is one of the best tasting things I know.

There is a good evolutionary explanation for this “food neophobia” (fear of new foods). In our evolutionary history, the story goes, there was a big risk associated with trying a new food. It might make you sick, or even kill you. So our brains evolved to bias us against trying new foods. It would not make sense for our brains to completely block us from new foods, but it would make sense to favor the familiar over the novel, when familiar foods were available, at least.

It makes a good story, but like most evolutionary explanations, it is difficult to test directly. We cannot observe or recreate the time in our genetic history when such a bias would have emerged. But one prediction of this evolutionary story is testable: If food neophobia is an evolved trait, then it ought to be represented in the genes.

So how do you test if something has a genetic basis? Even with the human genome project, we can’t just look at s strand of DNA and say, “there is the gene for avoiding new foods.” The first step, usually, is just to establish a correlation.

There are a lot of methods to do this, but a very popular one is twin studies. Identical twins have all their genes in common, because they both came from the same sperm and egg, which happened to split in two following fertilization. Non-identical, or franternal twins, come from different eggs and sperm. There just happened to be two eggs fertilized at the same time, but the people that result are no more genetically alike than any other sibling pair. Since the way we look is largely based on genes, identical twins look strikingly similar to each other, but fraternal twins look only somewhat alike. Indeed if any trait turns out to be extremely similar in identical twin pairs, but less alike in fraternal twin pairs, that is good evidence that the trait has a genetic basis.

That is the logic behind recent research led by Lucy Cooke, which suggests that differences in food neophobia are genetically based. They looked at thousands of twin pairs. They had parents answer a questionnaire which assessed each child’s reluctance to try new foods. Then they looked at how correlated the identical twins were on this measure. That correlation was very high, indicating that if one twin was high or low on food neophobia, the other was likely to be also. They also looked at the correlation in non-identical twin pairs, which was lower, though still correlated. This pattern of higher correlation in the identical twin pairs indicated that variations in the food neophobia trait were largely based on genetic differences, and not differences in child-rearing. You can read the abstract here.

These researchers went as far as to estimate the heritability of food neophobia: 78%. That is to say, they estimate that in the population they tested (British schoolchildren who are twins), 78% of the variability in food neophobia can be attributed to genes, and the remaining 22% to non-shared environmental factors. (Since the twins grew up in the same houses with the same parents, it would not make sense to attribute any of the variability to shared environments, which should be making them more alike, not more different.)

Without other studies with other populations and in different environments, it would be a mistake to generalize this heritability estimate to other groups. It seems likely to me that in countries where a lot of people go hungry while others are well fed, that differences in food neophobia would be largely attributable to environmental factors. Kids who do not get adequate nutrition are likely to eat what an adult gives them, whatever their genetic make up.

So what does this suggest about getting kids to eat exotic foods? Actually, Dr. Cooke emphasizes that parents can overcome children’s fear of new foods by making them familiar. Maybe serving a nibble of sushi every once in a while, or letting them eat the yummy rice in paella without forcing the shellfish on them will make those foods seem less threatening, without creating confrontations that only heighten their resistance. Maybe all that parents have to do is model adventurous eating for their kids, all the while serving them the same old macaroni and cheese, pizza, and peanut butter sandwiches. After all, they will have plenty of time to enjoy a wider range of foods when they are adults.

Does marijuana make you crazy?

Anyone who has ever seen “Reefer Madness” or survived a middle-school drug education program has probably figured out that there are a lot of exaggerated fears and warnings when it comes to marijuana. And all that hyperbole has evidently not done a lot to reduce the number of kids smoking pot, according to the latest survey.

But recent research has revealed a possible danger in pot smoking that really ought to worry potential users: It might increase your chances of becoming schizophrenic, or otherwise psychotic. Of course, this does not refer to the temporary effects that cause intensive sensory experiences, the illusion of profound thoughts, and an insatiable craving for brownies. The fear is that in some people, marijuana use may trigger a predisposition to a serious mental illness.

Not everyone is buying the argument that the association between marijuana use and psychotic disorders is cause and effect. A student commentary from Drexel University, for example, points out that the purported correlation is small, and that correlation does not imply correlation anyway. Bloggers Paul Armentano and Mitch Earleywine add that there is no new data in this study, only an analysis of previously published data. They also point out that the rate of schizophrenia is remarkably similar from one country to another, despite different patterns of drug use. But I would not go lighting up a joint to celebrate these counter arguments just yet.

Consider first the argument that the relationship is not a whopping correlation, but rather a small but significant correlation. This is exactly what we should expect, if only a small percentage of the population is vulnerable to schizophrenia and similar mental illnesses in the first place. And because the numbers are small relative to the population, we can’t expect big variations in the overall rate of schizophrenia, drugs or not. And the fact that they found this relationship in old data that looked at the broad population, rather than a new study looking at a targeted at-risk population should make us more afraid, not less afraid.

What this meta-analysis is saying is that the relationship between marijuana use and psychosis is strong enough to show itself even in studies that were never designed to look for it. I’m sure someone out there is running a study right now that focuses on teenagers with a family history of psychosis. If there really is a cause and effect relationship, in which marijuana use triggers a pre-exisiting vulnerability to psychosis, this is the type of study that should show big effects.

And what about the argument that correlation does not imply causation? I’m certainly glad that Mr. Gero and others have kept this in mind. Many science news writers seem not to be able to figure out the difference between a cause and effect experiment and a correlational study. But we should also remember that correlation does imply some sort of relationship. I tell my students to think of the two variables in a correlation as X and Y, and to get in the habit of considering three possibilities: X causes Y, Y causes X, or another, third variable (Z) causes both X and Y. In this story, the X causes Y hypothesis is that pot smoking causes psychosis (but probably only in those with a pre-existing vulnerability). The Y causes X hypothesis is that psychosis causes pot smoking. I think we can probably reject this, since the people in question were smoking pot before they became schizophrenic or otherwise mentally ill. A variation on this is not out of the question, though. Perhaps people who are destined to become schizophrenic are already unusual in a way that makes them more likely to smoke marijuana. This is very similar to the Z causes X and Y hypothesis, that some people have a pre-existing condition that makes them vulnerable to both marijuana use and schizophrenia. I see no reason why the first and last hypothesis could not both be true.

So what is the take home message? Should you worry that you might be one of those people for whom pot smoking could cause a lifetime mental illness? If there is a history of schizophrenia in your family tree, the answer is undoubtedly yes. The problem is that it is impossible to be sure that you are safe. We don’t know what might cause the vulnerability, but it is probably in the genes. Even if you don’t know of any schizophrenic relatives, that does not mean that none of your relatives were carrying some of the genes that lead to vulnerability. I hate to sound like a doomsayer, but it is difficult to rule out the possibility that you may be carrying genes that make you vulnerable. In the end, it is a roll of the dice. To me, the payoff seems pretty small in comparison to the risk.