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

It's All About Timing: Circadian Rhythms and Behavior

Anyone who has ever tried to drastically alter his or her sleep schedule (e.g. going from working days to working nights) knows that it is one of the more difficult biological tasks we can take on. Even altering one’s sleep patterns by a couple of hours (such as the shift experienced by cross-country travelers) can be disruptive, and enough to make us feel tired, mentally unclear, and grumpy. But why are we so inflexible when it comes to our daily routine? Why are our otherwise diverse bodies so sensitive to an adjustment of our biological clocks by just a few hours? Perhaps it is because millions of years of evolution have led to a daily body clock so fine-tuned that this sensitivity is adaptive.

Circadian (from the Latin for “around” and “day”) rhythms are endogenous biological patterns that revolve around a daily cycle. They are found in all organisms that have a lifespan that lasts more than a day. They are adaptive in the sense that they allow an organism to anticipate changes in their environment based on the time of day, instead of just being a passive victim to them. Thus, to foster that readiness, they usually involve the coordination of a number of physiological activities, such as eating/drinking behavior, hormonal secretion, locomotor activity, and temperature regulation.

A major nucleus of the mammalian brain, located in the hypothalamus and called the suprachiasmatic nucleus (SCN), is responsible for acting as the master time-keeper in mammals. When the SCN is lesioned (i.e. in rodents), it results in a complete disruption of circadian rhythms. The animals will demonstrate no adherence to a daily schedule, sleeping and waking randomly (although still sleeping the same total amount of time each day).

The SCN receives information from ganglion cells in the retina, which keep it appraised of whether it is light or dark out, and maintain its synchrony with a diurnal schedule. It is not, however, completely dependent on visual input for keeping time. A number of other environmental cues, such as food availability, social interaction, and information about the physical environment (other than light) are thought to play an important role in the SCN’s ability to maintain regular daily rhythms.

Although the SCN is the center for circadian rhythms, it seems that many individual cells are not directly controlled by the SCN. Instead, they are thought to maintain their own time-keeping mechanisms. Known as peripheral oscillators, these cells are present in a number of organs throughout the body, and can be sensitive to environmental cues as well as the signals of the SCN.

So, how do the neurons of the SCN actually “keep time”? They appear to be controlled by a cycle of gene expression that consists of a natural negative feedback mechanism. The following is a simplified version of this mechanism. Cells in the SCN produce a protein known as CLOCK (circadian locomotor output cycles kaput). This protein binds together with another, BMAL1, and they act as a transcription factor, driving the synthesis of the proteins period (PER) and cryptochrome (CRY). When large amounts of PER and CRY have been created, they form a complex and inhibit the activity of CLOCK/BMAL1---thus inhibiting their own production. Gradually, PER and CRY proteins degrade, allowing CLOCK and BMAL1 to begin promoting the production of PER and CRY again. The cycle consistently takes around 24 hours to complete before it repeats, allowing the clock in the SCN to oscillate on a regular circadian rhythm.

Disorders of the SCN can result in disruptive sleep problems, such as advanced sleep phase syndrome (early sleep and wake times) or delayed sleep phase syndrome (preference for evenings and delayed falling asleep). More attention is now being focused on the role a dysfunctional circadian system may play in already identified behavioral problems. A recent review in PloS Genetics examines the potential influence circadian rhythm disturbances may have in disorders like depression, schizophrenia, and even autism.

Circadian disruptions are present in all major affective disorders, including depression, bipolar disorder, and schizophrenia. Although the exact role circadian rhythms play in these disorders is not yet known, it may be substantial. This is supported by the influence changes in sleep patterns can have on the alleviation of primary symptoms of these disorders. For example, sleep deprivation has been demonstrated to have an antidepressant effect (albeit short-lived) in patients. And some affective disorders, such as seasonal affective disorder, seem to have a basis in the length of the day, and shape emotional states.

Autism spectrum disorders (ASD) are correlated with low melatonin levels, and a gene responsible for the synthesis of melatonin is considered a susceptibility gene for autism. Mice with a mutant form of this gene demonstrate deficits in social interaction, anxiety, and increased occurrence of seizures. It is postulated that behavioral problems in ASD may be influenced by the failure of an individual’s circadian clock to effectively take note of social and environmental cues.

Variants of a number of time-keeping genes, such as PER1, CLOCK, and CRY have been found to be associated with behavioral disorders. It has yet to be determined if these variations are causative, contributive, or unrelated to the disorders. Keeping in mind how influential a disturbance of circadian rhythms can be in our daily lives, however, it seems logical to investigate the possibility of their contribution to pathologies.

Barnard, A.R., Nolan, P.M., Fisher, E.M. (2008). When Clocks Go Bad: Neurobehavioural Consequences of Disrupted Circadian Timing. PLoS Genetics, 4 (5), e1000040. DOI:10.1371/journal.pgen.1000040

Read more about the suprachiasmatic nucleus: Know your brain - Suprachiasmatic nucleus

Changes in Gene Expression and Addiction

As I discussed in a post last week, addiction seems to correspond to abnormalities in dopamine (DA) transmission throughout the reward areas of the brain. Specifically, initial uses of a drug tend to correlate with low levels of dopamine receptor availability in the nucleus accumbens (NAc), while long-term use affects DA transmission throughout the entire striatum (the NAc is located in the ventral portion of the striatum, or the part nearer the front of the brain).

The striatum is a subcortical region of the brain, and part of the mesocorticolimbic DA pathway, which is integral to the evaluation and appreciation of rewards (like drugs). Striatum is from Latin, and means striped. It is so named because the entire region has a striped appearance, due to the alternating bands of gray and white matter that make it up.

The changes that occur in the striatum are postulated to be responsible for the long-lasting behavioral changes that drug addicts can experience, such as cravings for drug use, an inability to enjoy previously rewarding experiences, and proneness to relapse. It has been suggested that these changes must be preceded by some sort of synaptic remodeling in order to have such a long-lasting effect, and those synaptic changes could be a result of fluctuations in DA transmission. How exactly they occur, however, has yet to be elucidated.

A study to be published in an upcoming issue of Nature may shed some light on the mechanism behind these changes. It involves gene expression, and a phosphoprotein known as DARPP32 (dopamine-and cyclic AMP-regulated phosphoprotein with molecular weight 32 kDa).

A phosphoprotein is a protein that has had a phosphate group attached to it, through a process known as phosphorylation. Phosphorylation is an important event in cells, as it often is the catalytic process that activates enzymes and receptors. Dephosphorylation can “turn off” these enzymes, and involves proteins called phosphatases.

When dopamine 1 receptors (D1R) are stimulated, they in turn activate DARPP32, which inhibits a phosphatase known as protein phosphatase 1 (PP1). This signaling cascade affects the phosphorylation of numerous proteins in the cytoplasm and nucleus of a cell.

In the Nature study, the researchers found that the administration of amphetamine, cocaine, or morphine to mice caused DARPP32 to accumulate in the nuclei of striatal neurons. Further studies of neural cultures indicated that dopamine prevents a specific DARPP32 phosphorylation site, Ser97, from being phosphorylated. Ser97 appears to be responsible for exporting DARPP32 from the nucleus of the cell, thus DARPP32 builds up inside the nucleus.

When DARPP32 accumulates in the nucleus, it causes the phosphorylation of a histone, H3. Histones are proteins that DNA winds around to make chromatin, the protein and DNA complex that makes up chromosomes. Phosphorylation of histones often affects chromatin structure, and gene expression as a result.

Mice with mutations in the Ser97 site demonstrated long-lasting aberrations in their behavioral responses to drugs and other rewards. They showed decreased acute locomotor responses to morphine administration, along with a reduced locomotor sensitization to cocaine. Their motivation to obtain a food reward was also diminished.

Thus, this signaling pathway may be responsible for one of the most potent behavioral changes in addiction, when euphoria achieved from the drug diminishes along with the pleasure once obtained from other rewards. This change can contribute to compulsive drug seeking, as an addict obsessively continues to seek the pleasure once associated with their drug of choice. If altered gene expression is responsible for these changes, it would help to explain why they can persist for such a long period of time after the cessation of drug use—sometimes continuing to affect the behavior of an addict for years, and often making their efforts to stay sober much more difficult.