Why do I procrastinate? I'll figure it out later

Procrastination

If you are a chronic procrastinator, you're not alone. Habitual procrastination plagues around 15-20% of adults and 50% of college students. For a chronic procrastinator, repeated failure to efficiently complete important tasks can lead to lower feelings of self-worth. In certain contexts, it can also result in very tangible penalties. For example, a survey in 2002 found that around 40% of American tax-payers procrastinated on their taxes, resulting in errors due to rushed filing that cost an average of $400 per procrastinator. More importantly, we tend to procrastinate when it comes to medical care (both preventive and therapeutic), which can involve very real costs to our well-being.

Why is the urge to procrastinate so strong? It sometimes seems that we are compelled to procrastinate by a force that is disproportionate to the small reward we may get from putting off a task we're not looking forward to. According to Gustavson et al., the authors of a study published last week in Psychological Science, a predisposition to procrastinate may have its roots in our genes.

Previous research has suggested a potential link between a tendency to procrastinate and an impulsive nature. Gustavson et al. explored this possible connection by observing the traits of procrastination and impulsivity in a group of 181 identical and 166 fraternal twins. Because identical twins share 100% of their genes and fraternal twins only share around 50% of their genes, if a trait is shared by identical twins more frequently than it is by fraternal twins, it suggests the trait has a significant genetic basis (for more on twin studies see this post).

The investigators reported a significant correlation between procrastination and impulsivity (r = .65). The group also reported that their genetic model determined that procrastination and impulsivity were perfectly correlated (r = 1.0), suggesting that the genetic influences on procrastination and impulsivity might be completely shared. In other words, according to this study, there are no genetic influences on procrastination that aren't also affecting impulsivity.

But why would these two traits be associated with one another? Procrastination involves putting things off, while impulsivity involves doing them on a whim. Gustavson et al. suggest that both procrastination and impulsivity involve a failure in goal management and a deficit in the ability to guide behavior effectively using goals. The authors refer to a hypothesis proposed by procrastination researcher Piers Steel that suggests impulsivity may have been adaptive to our ancient ancestors when survival depended more on thinking and acting quickly. In today's much safer world, however, planning for events yet to come has superceded impulsivity in terms of importance.

Thus, like many of our other bad habits, procrastination may have its roots in a behavior that was at one point adaptive and is now outdated. So, if it feels like your desire to procrastinate is driven by a force much stronger than your willpower, it may be so. If Gustavson et al. are correct, the impetus for procrastination lies in genetic programming that dates back to the Pleistocene era.

Gustavson, D., Miyake, A., Hewitt, J., & Friedman, N. (2014). Genetic Relations Among Procrastination, Impulsivity, and Goal-Management Ability: Implications for the Evolutionary Origin of Procrastination Psychological Science DOI: 10.1177/0956797614526260

Is your biological clock ticking? Maybe you should ignore it

As I've transitioned into middle age, I've gotten used to seeing my Facebook feed filled with baby pictures, descriptions of charming family outings, and adorable quotations from the mouths of toddlers. If I knew nothing about what it were like to have a child (mine is just finishing up the terrible twos), I would assume from scrolling through these perfectly tailored social media portraits of others' lives that having kids is a non-stop fun-filled procession of treasured moments. Of course, this perspective is not confined to my Facebook news feed. It's common knowledge that children make us happier and help us to feel more fulfilled.

This is one of many instances, however, where research and folk wisdom don't mesh. In fact, when studies have compared the happiness of those with children to the happiness of those without children, they have often found that having children is associated with lower life satisfaction. A recent publication looked at data from close to 1.8 million Americans and over a million other respondents throughout the world. What the researchers (a psychologist and an economist--both from Princeton) found generally supported the idea that those who have children are not as happy as those who do not.

There are many explanations for such a finding other than the hypothesis that kids make us miserable. For example, although the survey data used by the Princeton researchers indicated lower life satisfaction in people with children, people with children also experienced less physical pain, felt they had more enjoyment in their lives, earned higher incomes, were better educated, and were healthier. On the other hand, they experienced more stress, worry, and anger. Thus, it may be that having children generates its share of highs and lows, causing us periods of intense stress and upset that are relieved by the enjoyment we get from spending time with our kids. Most parents would probably agree with this statement to some extent.

Regardless, if the data indicates that people with kids are--in a best case scenario--no happier than those without, then where do we get this idea that having kids will make us happier? And why, when we talk to people with kids (or see their posts on Facebook), are we given the distinct impression that a life without children is somehow...lacking?

 

Survival of the Fittest

The answer to this conundrum may involve evolution. Of course, because having children is the only way to directly pass on one's genetic lineage, then the act of having children causes the propagation of a genetic makeup that may predispose someone to look favorably upon having children. In other words, if there were genes that affected someone's personality in such a way that they loathed the idea of having children, then those genes wouldn't last very long in the population because the reluctance of those who possessed them to have children would naturally limit their propagation.

Although genes that predispose one for parenthood may be part of the answer to this puzzle, there also may be a role for another unit of transmission: the meme. The term meme was coined by Richard Dawkins in his revolutionary book about genetics called The Selfish Gene. A meme is an idea. The idea can be represented by a cultural norm, a style, a behavior, or anything else that can be spread from person to person and generation to generation. Just like genes, however, memes are subject to natural selection.

For example, the rock group Bad English recorded a song 25 years ago called "When I See You Smile." You may or may not remember this song depending on your age and how often you listened to top-40 music in 1989. Here's a link to the video if you care to refresh your memory and/or reminisce. Bad English's song could be considered to have moderately good "fitness" as a meme. It was an idea that enjoyed brief popularity, and at the height of its popularity a significant percentage of the world's English-speaking population was aware of its existence (and maybe even sung along once or twice). However, I don't expect anyone will be singing it 100 years from now.

In contrast, the lyrics to Auld Lang Syne came from a Robert Burns poem written way back in 1788. Over 225 years later, the song is known in many countries throughout the world and sung regularly at events like the beginning of the new year or any other occasion that signals the end of a period of time (e.g. funerals, graduations). The song is easy to remember, has a meaning (the symbolism of endings and beginnings) that resonates with people regardless of their culture, and is sung to a tune that is easy to reproduce. Auld Lang Syne is an extremely "fit" meme.

Although songs may be somewhat trivial examples of memes (contrasted with examples like organized religion or language), the difference between the longevity of these two songs suggests that some memes seem to be better at replicating than others. With that in mind, lets turn back to the idea that having children is an enriching experience. There isn't a much better way for a meme to ensure its survival than if holding it as a belief makes people more likely to engage in behavior that will lead to its own propagation. Believing in the idea that children bring happiness makes one more likely to have children. Those offspring then provide another set of impressionable minds who are readily convinced by their child-having parents and grandparents that children are the greatest source of joy in the world. And the meme continues to spread.

Genes don't necessarily have to promote health to allow them to continue to be propagated, but they have to have some quality that promotes their own transmission. Memes work the same way. They don't need to be accurate ideas, but there has to be something driving their dissemination. Could it be that our belief in the wonder of childbearing is simply due to the success of this meme in promoting its own transmission?

It's possible. As Daniel Gilbert discusses in his investigation of the errors we commit in deciding what will make us happy, Stumbling On Happiness, it would not be the first meme that led us astray. For example, the meme that great wealth leads to happiness continues to thrive throughout much of the world. Evidence suggests, however, that once one has enough money to ensure one's basic needs are provided for, additional money does little to contribute to one's satisfaction.

So, if you're childless and experiencing pangs of jealousy over the seemingly perfect family photos your friends are posting to Facebook, remember that the research suggests your friends aren't as happy as they look in those photos. And maybe you don't have children because you just haven't been suckered into the mass delusion that children will make your life complete.

Deaton, A., & Stone, A. (2014). Evaluative and hedonic wellbeing among those with and without children at home. Proceedings of the National Academy of Sciences, 111 (4), 1328-1333 DOI:10.1073/pnas.1311600111

Why You Can't Remember Where Your Keys Are

Why do we remember? To some this might seem like a ridiculous question. Memory is so intricately intertwined with our conception of existence that it is difficult to objectively ask questions about why we developed the capacity for it, or to imagine the possibility of a life without it. If one is to assume, however, that like every other facet of the human condition, memory evolved from rudimentary beginnings, then “why do we remember?” becomes not only a reasonable question, but an important scientific inquiry.

Looking at memory from an evolutionary standpoint, one must assume that it developed to serve an adaptive purpose. Of course, when one begins to cogitate on what that purpose might be, it is easy to stumble into purely speculative territory. Evolutionary psychologists have received much criticism for this. Examples of hypotheses about evolutionary origins gone wrong shouldn’t serve to negate the efforts of the entire field, however, it should just encourage a more cautious approach.

Two psychologists from Purdue University, James Nairne and Josefa Pandeirada, published an article in this month’s Current Directions in Psychological Science that describes their lab’s approach to the evolution of memory. It attempts to avoid blatant speculation by beginning with simple hypotheses about the purposes of memory, and testing their validity before moving on to more complex explanations.

They start with three basic assumptions that an evolutionarily adaptive perspective on memory would require. The first is that memory probably didn’t evolve just to recall the past. In other words, memory must serve a purpose, allowing us to predict the probability of future events given certain circumstances. Second, memory should be governed by priorities. We shouldn’t remember all environmental stimuli with equal clarity. This would lead to a maladaptive inability to remember the most salient stimuli, and would clutter our memories with unimportant details about our environment. Third, memory should assign the highest salience to environmental stimuli that improve reproductive fitness and evolutionary adaptiveness. So, those things in our environment that have historically proven to be the most important for survival should garner the most mnemonic attention.

Based on these assumptions, Nairne and Pandeirada conducted behavioral experiments to determine if survival-related processing enhances retention. After an initial study indicated that participants were able to remember survival-related words better than other words that required a similar level of processing, the researchers designed a large study that compared survival processing to some of the most renowned mnemonic techniques, like imagery and the use of autobiographical cues. They found that survival processing resulted in higher average recall rates than any of the other techniques tested.

So perhaps we remember because it allows us to predict where danger might lie, who we can trust, successful ways to court a mate, how to obtain food, etc. Maybe this seems obvious, but it only becomes so with a little thought. Our inherent predisposition toward an anthropocentric view of the world often causes us to unconsciously regard our mnemonic abilities as above the laws of science and the progression of evolution. We don’t usually think of our memory as evolving in the same way that our bodies have, but the idea that we have developed context-specific cognitive modules through evolution is becoming hard to ignore. Then again, perhaps there is a reason we have a tendency to ignore such explanations for our cognitive abilities. Anthropocentrism may be adaptive in its own right.

 

Nairne, J.S., Pandeirada, J.N. (2008). Adaptive Memory: Remembering With a Stone-Age Brain. Current Directions in Psychological Science, 17 (4), 239-243. DOI:10.1111/j.1467-8721.2008.00582.x

The Evolution of Schizophrenia

Schizophrenia is one of the more frightening and debilitating mental disorders. It can cause hallucinations, delusions, and social withdrawal, as well as a variety of other cognitive afflictions. While scientists have yet to decipher the etiology of the disease, its high inheritability rate (60-85%) has led many to look for answers in genetics. Since schizophrenia affects cognitive functions that are distinctly human (like language-related abilities), some have begun to consider ways in which the human brain has evolved, and how this could shed light on the causes of schizophrenia.

A group of researchers published a study this week in Genome Biology that examines the relationship between schizophrenia and the evolution of higher order processes in humans. They first investigated the evolution of molecular mechanisms involved in human cognition. Then they examined the changes that occur in schizophrenic patients, and looked for an overlap between the two data sets.

They found that, of 22 biological processes that show a strong indication of recent positive selection, 6 involve disproportionate numbers of genes that are implicated in schizophrenia. All of those 6 are implicated in energy metabolism, or the regulation of energy flow through the body/brain.

The group then performed comparative analyses between schizophrenic patients, healthy controls, chimpanzees, and rhesus macaques. The reason other primates are used in such a study is to further delineate the evolutionary picture. If an evolutionary change in the brain can be found between a human and a chimpanzee, for example, then one can assume it was a human development that took place after the divergence of chimps and humans.

The researchers saw distinct differences between the four groups, indicating recent evolutionary changes. They again found that metabolites that play key roles in energy metabolism (e.g. lactate, glycine, choline) were affected.

These results caused the scientists to suggest that recent evolutionary changes in our brain’s energy metabolism may have been integral in the development of the higher order processes we associate with the human brain. These changes would have been necessary to meet increased energy demands as the brain went through increases in size, number of synaptic connections, extent of neurotransmitter turnover, etc.

It seems that brain energy metabolism is negatively affected in disorders like schizophrenia. For example, decreases in blood flow to the prefrontal cortex have been reported when schizophrenics attempt cognitive tasks. The researchers in this study suggest that, after the last 2 million years of rapid evolution, the human brain is basically pushing the limits of its metabolic abilities. Thus, any aberrations in the brain’s energy metabolism capabilities could have drastic results, schizophrenia being one example.

According to this perspective, schizophrenia is a by-product of our rapidly evolving brains. Because we are operating at near-capacity levels, any reduction in our ability to produce and process brain energy can be debilitating. In order to verify this hypothesis, however, much more work examining the correlation between evolution, energy metabolism, and brain disorders will need to be done.

 

Khaitovich, P., Lockstone, H.E., Wayland, M.T., Tsang, T.M., Jayatilaka, S.D., Guo, A.J., Zhou, J., Somel, M., Harris, L.W., Holmes, E., Paabo, S., Bahn, S. (2008). Metabolic changes in schizophrenia and human brain evolution. Genome Biology, 9 (8), R124. DOI:10.1186/gb-2008-9-8-r124

Dopamine and the Bruce Effect

If you take a recently impregnated female mouse and place her in a cage with an unfamiliar male, something curious often happens. The female, upon smelling the new male's urine, spontaneously aborts the fetus as her body drastically reduces its production of prolactin (PRL), a hormone responsible for progesterone secretion and thus essential to maintaining a pregnancy. The embryo fails to implant and the female begins ovulating again, making her receptive to copulation attempts by the new male. This strange phenomenon was first noticed by biologist Hilda Margaret Bruce in 1959, and is referred to as the Bruce effect.

The Bruce effect has been a curiosity to biologists since its discovery, as many have sought to explain why the female mouse’s body would seemingly be programmed to destroy her own offspring. After all, isn’t reproduction supposed to be the “goal” of evolution, and thus of life?

Several explanations have been offered to make sense of the Bruce effect. One is that it is an adaptive mechanism to protect the female’s potential maternal investment from being lost to infanticide. Infanticide is a fairly common practice among many species, and is usually committed by the male.

A male often cannot visibly determine if a female is pregnant when he encounters her (if her fertilization has been recent). Thus, upon copulating with her, he takes a risk that she may already be pregnant. If she were to produce offspring from another male, he might mistake them for his own and invest his resources in raising them (whatever “raising” may mean in the particular species). The risk being, if they are not his offspring he makes the investment but does not gain the benefit of his genes being passed on to a new generation. This is evolutionary suicide, and some biologists believe the males of many species instinctually go to great lengths to avoid it.

One way to make sure none of one’s resources go to raising another’s offspring is to simply get rid of the offspring. Male mice will frequently be infanticidal for the first three weeks after copulating with a female. Then they act paternally for about two months, after which they regress to their infanticidal tendencies. Coincidentally (not really), the mouse gestation period is three weeks and the weaning period is about two months. So the male times his infanticidal behavior perfectly to ensure that any offspring he helps to wean are his (note again that this is instinctual, not conscious behavior).

So, many biologists have suggested the Bruce effect may be a way for the female to avoid going through a pregnancy and investing all of her resources in it, just to have her progeny killed by a new male. Instead, she can abort the fetus and be receptive to him, in the process ensuring that she will have the opportunity to raise offspring into adulthood.

An alternative explanation for the Bruce effect involves mate selection. In this hypothesis, blocking the pregnancy is beneficial to the female by providing her with a novel mating partner. In highly territorial animals like rodents, a female may be more inclined to mate with the mouse whose urine she can currently smell, as he is most likely dominant in that territory.

Whatever the reason for the effect, a female also seems to reach a point when she has too much invested in the pregnancy already for it to be beneficial to abort. In mice, this occurs after the first few days of pregnancy, when the embryo becomes implanted. After this point, the Bruce effect no longer occurs. This is thought to involve a type of evolutionary weighing of the pros and cons. After three days of pregnancy, the female “decides” she has put enough time into her fetus that it would be counter-productive to start over. She must take the risk.

While the evolutionary cause of the Bruce effect may not be known for some time, a study published in July's Nature Neuroscience brings us closer to understanding the neural mechanism behind it. It seems to be dependent upon the versatile neurotransmitter dopamine.

When the female mouse smells another male’s urine, two sense organs in the nasal cavity are involved in processing the scent. One, called the vomeronasal organ (VNO), has pheromone-sensing capabilities. The other, the main olfactory epithelium (MOE), detects odorants. Both organs project fibers to the main olfactory bulb (MOB) and accessory olfactory bulb (AOB). The MOB contains a large population of dopaminergic interneurons, known as the juxtaglomerular dopaminergic interneurons (JGD).

As these dopamine interneurons are highly involved with olfaction, the scientists involved in the study wondered if they might also play a role in blocking pregnancy through urine odor detection. When they measured dopamine levels in the female mouse brain, they found a surge in dopamine occurred after the third day of the pregnancy—the time at which male odor no longer has an abortive effect on the fetus.

When they administered a dopamine antagonist, which blocks dopamine transmission, spontaneous abortion again occurred, even after implantation on the third day. Therefore, dopamine appears to interfere with the perception of the male urine odors, and is responsible for the suppression of the Bruce effect after the third day of a mouse pregnancy.

These findings represent a new understanding of the roles of the olfactory bulb, implicating it in the control of reproduction and social behavior in rodents. While not really applicable to humans, making sense of the Bruce effect is important in comprehending social behavior that, without knowledge of evolutionary theory, seems otherwise inexplicable.

 

Che Serguera, Viviana Triaca, Jakki Kelly-Barrett, Mumna Al Banchaabouchi, Liliana Minichiello (2008). Increased dopamine after mating impairs olfaction and prevents odor interference with pregnancy Nature Neuroscience, 11 (8), 949-956 DOI:10.1038/nn.2154