Understand Your Stress

I recently started writing for berkeleyByte, a student-run website on design, culture, and technology.

My most recent article discusses how stress can lead to depression and how you can prevent it.

http://www.berkeley byte.com/2013/12/12/understand-your-stress



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Anorexia Nervosa












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Understanding Narcolepsy


This short video shows narcolepsy in canines. The disorder has been observed in research in mice, rats, dogs, and horses. Although these cases develop with slight deviations from the human form, they are instructive for better comprehending the overall causes, symptoms, and treatments.

But one research tool in narcolepsy is particularly exciting because it could affect the clinical analysis of the disorder in the near future. Traditionally, narcolepsy is observed in animals and human patients by connecting electroencephalogram (EEG) electrodes to the individual’s skull. Using a monitor, a researcher may examine the different brain waves and when they occur. On the EEG recordings, narcolepsy appears as long strands of rapid eye movement (REM) brain activity that is not preceded by deep slow-wave sleep. (Narcolepsy pertains to problems in REM sleep. A narcoleptic patient falls abruptly into REM sleep while he is awake.)

In animals, such as mice, observing narcolepsy can be time-consuming and difficult because of the tiny electrodes that must be implanted in the skull without damaging any of the disorder’s physiological manifestations. The process for classifying sleep stages is also laborious, especially since a researcher must manually read through the squiggly array of brain wave activity in order to correct any classification errors conducted by the computer software.

Fortunately, there may be a solution to these problems because the jagged REM brain waves are not the only way to ascertain a period of narcolepsy. The piezoelectric (PZT) system has long been known for its environment-promoting technology in converting vibrations into electrical energy. Recently, the sensory device has diversified its uses as researchers experiment with it for analyzing sleep disorders such as narcolepsy. Future endeavors pertaining to PZT may not only boost animal safety but even accelerate studies on sleep.

More specifically, because the PZT monitor discerns motion, it can potentially be used as a noninvasive method for observing cataplexy in narcoleptic experimental animals such as mice. Recent studies demonstrate the PZT’s ability to record the animal’s heart and respiration rates as it is lying down. The device consists of a metal platform with sensors. When a narcoleptic mouse has a bout of cataplexy, it collapses and lies flaccidly against the platform. The PZT sensors, aligned beneath the surface, then detect the mouse’s heart rate and record it. These sensors can potentially discern between a normal resting period and a real case of cataplexy within the mouse due to differentiations between the two heart rates. While the invasive EEG relies on brain activity and algorithms to classify the mouse’s sleep stages, the passive PZT may more accurately catalog instances of cataplexy, which could revolutionize research in narcolepsy for all mice, experimenters, and human patients (Sagawa et al.).

PZT is now only tested on mice and may help in animal experiments for trialing narcolepsy treatments in the future. However, it may soon replace the EEG methods of recording human brain activity. Perhaps someday, researchers will attach a small PZT monitor to the narcoleptic patient’s chest in a far simpler manner of observing the disorder in humans.

Despite recent advances, narcolepsy has only recently become a cutting-edge frontier in sleep research. It was first described in medical literature in 1877, and it now only appears in 0.05% of the world population. Therefore, it is no surprise that its causes and cures are still hazy (Mignot).

It is specifically a sleep disorder characterized by an individual’s distorted circadian rhythm and short bouts of paralysis and hallucinations. The patient displays excessive daytime sleepiness (EDS) in the form of sleep attacks, in which he feels a strong urge to take a short nap during the day. Insomnia consequently occurs at night. As implied by the PZT experiments, cataplexy is also a common symptom of narcolepsy. It consists of abrupt periods of muscle weakness or paralysis effected by extreme feelings of positive emotions (such as excitement or surprise). Such periods of cataplexy may last anywhere from a few seconds to one minute (Montagna and Chokroverty 119).

Narcolepsy also has slighter symptoms that may be discerned only by the patient. A narcoleptic often has sleep paralysis, in which he may be paralyzed at the onset of sleep, during a short moment of wakefulness at night, or upon awakening in the morning. During these moments of paralysis, he may have extreme frightening hallucinations that will only terminate by some external stimulus. At the physiological level, narcoleptics may have a lower blood pressure and body temperature. They are almost always obese although they ingest less food than normal (Montagna and Chokroverty 121).

Evidently, at the neuronal level, there must be a multitude of dysfunctions for so many threatening symptoms to occur at once. Yet this point is also where narcolepsy faces resistance because of crucial knowledge that current researchers lack. Scientists know that the disorder revolves around the neurotransmitter orexin (also called hypocretin), which regulates feeding and sleep. Narcolepsy occurs when there are low or no levels of orexin being circulated through the brain (Mignot).

The orexinergic neurons based in the lateral hypothalamus deteriorate at some point during the narcoleptic individual’s life, which causes the onset of the disorder. Because of this abrupt neuronal apoptosis, narcolepsy is likely an autoimmune disease. However, more proof is required to confirm this belief. (Carlson 229).

Normally, the orexinergic neurons fire during an individual’s daytime period of wakefulness and vigilance. Such firing presumably promotes alertness. Thus, due to the fewer orexinergic neurons that fire in a narcoleptic brain, the patient feels less awake during the day. At night, although there is conclusively less stimulation promoting wakefulness, the orexinergic effects of wakefulness are produced. Further research is still required to fully comprehend the reasoning behind this phenomenon.

This piece of information proves interesting because of narcolepsy’s apparent dissonance with the circadian rhythm’s traditional response to day and night. When we travel across the world, our circadian rhythms reset and adjust to the time zone. For example, if we are in China, which is about 12 hours ahead of America, the morning light acts as a zeitgeber to reset our physiological sense of time. But a narcoleptic, who has bouts of sleepiness during the day and insomnia at night in America’s time zones, will adjust to the new time setting but presumably continuing to have bouts of sleepiness in the day and insomnia at night.

So could there possibly be more at hand other than dysfunctions pertaining to the orexinergic neurons? Perhaps the suprachiasmatic nucleus (SCN), the primary controller of the human biological clock located in the hypothalamus, is a contributing source to the problem. In a similar autoimmune disease, maybe the SCN fails as a cause or effect of the orexinergic neuronal deterioration.

Narcolepsy has encountered a variety of semi-effective treatments, but current research proves that there is great hope for the future. Currently, the most common treatment is modafinil, a wake-promoting stimulant that works against EDS. Altogether, researchers have been investigating antidepressant drugs that fight against the REM sleep problems of narcolepsy. Such drugs promote serotonin and norepinephrine activity in the brain and can reduce the dysfunctions behind cataplexy, sleep paralysis, and hypnagogic hallucinations (Carlson 219).

In recent years, narcolepsy treatments have branched beyond the scope of traditional drugs. One such undertaking is hypocretin replacement therapy, which—as the name suggests—would reduce sleepiness and cataplexy by increasing orexinergic levels in the brain. In the therapy, the patient would be administered orexin receptor agonists through cell or gene transplantation. The agonists would promote the orexinergic effects and thus increase physiological alertness. Testing for this therapy is currently taking place (Nishino et al. 217-8).

From its coinage in 1880 to its correlation with orexin deficiency in 2000, human understanding on narcolepsy has developed immensely in the past 150 years. The disorder initially faced many roadblocks due to its rareness and the researching world’s lack of knowledge on the subject. Fortunately, the latter half of the twentieth century has passed with an increased interest in narcolepsy along with a forefront of hypotheses and features to test and dissect in the future. The ensuing century will doubtlessly solve many of the questions behind narcolepsy, with more possibilities for preventing the disorder and learning more about the circadian rhythm in the process.

Carlson, Neil R. Foundations of Behavioral Neuroscience. 8th ed. 2006. Boston: Allyn & Bacon-Pearson, 2011. Print.

Mignot, Emmanuel. “History of Narcolepsy.” History – Center for Narcolepsy – Stanford University School of Medicine. Stanford School of Medicine, 2001. Web. 21 Apr. 2012. <http://med.stanford.edu/‌school/‌Psychiatry/‌narcolepsy/‌narcolepsyhistory.html&gt;.

Montagna, P, and S Chokroverty, eds. Handbook of Clinical Neurology. Vol. 99. 2011. N.p.: Elsevier B. V., 2011. Print. 3.

Nishino, S, et al. “Hypocretin /‌ orexin and narcolepsy: new basic and clinical insights.” Acta Physiologica 198 (2009): 209-22. PDF file.

Sagawa, Yohei, et al. “Noninvasive detection of sleep /‌ wake changes in orexin /‌ ataxin-3 transgenic mice across the disease onset.” N.d. Microsoft Office PowerPoint file.


(A continuation from the previous post.)


















[2] Mandler, 55-60.

[3] James, 1.









[12] Mandler, 10.



February 21, 2012 1 comment
















[2] Myers, 8.



[5] Descartes, 182.


[7] Michael Rohlf, “Immanuel Kant,” Stanford Encyclopedia of Philosophy, accessed November 19, 2011, last modified May 20, 2010, http://plato.stanford.edu/entries/kant/.

[8] Alan Kim, “Wilhelm Maximilian Wundt,” Stanford Encyclopedia of Philosophy, accessed November 19, 2011, last modified June 20, 2006, http://plato.stanford.edu/entries/wilhelm-wundt/.





[To be continued.]

A Look at Transgender Brains

January 4, 2012 5 comments

In a culture where transgender individuals seem misunderstood or misrepresented, 14-year-old Nicole Maines has broken societal restraints in her burgeoning journey as a transgender. Born as Wyatt Maines, Nicole and her identical twin brother Jonas were reportedly “different” from the start of their youth. As a younger boy, Nicole had expressed interests in girlish activities, such as wearing heels and playing Barbies, while Jonas had always favored sports and action. The twins’ growing differences persisted as their parents tried to evaluate the seriousness and possible consequences of Nicole’s girlish tastes. By the end of elementary school, Nicole changed her name from Wyatt and grew out her hair. Finally, the family discovered the Children’s Hospital Gender Management Services Clinic, a center that uses hormone treatment to gradually alter an individual into the opposite gender.

The clinic’s process consists of hormone suppressers that the youth takes in order to counteract the hormones released from the gender he or she was born as. These chemicals’ effects are reversible; if the patient stops consumption, he or she can undo the major consequences. Upon reaching adolescence, if the person still feels inclined to continue the process, he or she receives the unalterable treatment for the hormones of the opposite gender. The final step in the process, occurring after age 18, is the gender reassignment surgery, in which the individual comes to physically be the opposite gender.

Because she was an identical twin, Nicole offers a unique case study for the transgender population. Her circumstances allude to the longstanding debate on nature versus nurture. But while environmental and psychosocial factors may have influenced Nicole to favor the opposite gender’s tastes, it seems more likely that her state has arisen from the “nature” perspective because of the early onset of her transgender preferences.

Various studies have supported the “nature” theory of transgender alignment through observations and comparisons within the brain. In specific examples, prior post-mortem studies have demonstrated the similarities in the brains of male-to-female (MtF) transgenders and those of control females. The overall brain sizes from both of these groups are relatively smaller than that of the average male. Furthermore, particular brain structures, such as the anterior hypothalamic nucleus, have displayed greater likenesses in female and MtF brains than with males’ brains with regards to structural volume and density. (Nonetheless, such post-mortem results are ambiguous because of these MtF individuals’ estrogen-consumption that may have influenced specific brain masses either during or after the brain’s primary growth and development. In this case, the brain differences may be due to either pure “nature,” the effects of estrogen treatment, or both.)

A recent study has solved the inaccuracy caused by the estrogen-consumption of MtF transgenders. In this study, the researchers found 24 MtF transgenders who planned on taking hormone treatment in the future. The individuals qualified for the experiment if they had the sex-determining region Y (SRY) gene, which is unique to males. The brains of these 24 people were compared to the brains of female and male control groups. Because the transgenders had not received any treatment in the past, the experiment’s outcome was reliable and noteworthy.

Generally speaking, studies state that female brains—although relatively smaller than male brains—have less gray matter and more white matter due to the extra folds (fissures and sulci) in their brains. (Gray matter is the softer outer region of the brain; white matter is the slightly harder inner mass.) However, several specific structures in female brains have a greater gray matter volume than corresponding structures in male brains. The study used these particular structures in their experiment as they compared the size of each of these masses throughout the three groups. The ultimate question was whether transgender brains would show greater similarities with the brains of the initial gender (which, in this case, was male) or with the brains of the preferred gender (female).

The study revealed that all three groups had different gray matter volumes for the specified brain structures. While females had greater gray matter volume for these brain structures than those of males, transgender individuals displayed unique average gray matter volumes that correlated with neither those of the males nor females. Their gray matter volumes were generally slightly greater than the structural volumes of the control males; volumes were also more similar to the males’ than they were to the females’ structural volumes.

The main exception to this finding was the putamen, a round brain mass located near the center of the brain. The putamen, part of the basal ganglia structure, performs functions relating to motor movements and learning. The structure’s average gray matter volume in transgender individuals was far closer to the females’ average volume than the males’. As the researchers concluded, the transgenders’ putamen was one of the few structures to be so “feminized.”

The experiment was altogether interesting because it demonstrated unique differences in transgender brains that evidently occurred only by “nature,” since none of the MtF individuals had previously engaged in hormone treatment. The results proved that these transgenders’ brains were structurally similar and distinct.

Nonetheless, more must be at hand than simply “nature” superseding “nurture.” After all, Nicole Maines is a transgender, but her identical twin brother is not. Despite their matching DNA, there were probably biological, physiological, or mental differences between the twins that caused Nicole to make her decision.

Their situation thus leads us to epigenetics, a new flourishing subject in psychology and neuroscience that may explain transgender characteristics and why they might occur in only one identical twin despite their prevalently “nature” quality.

The field might explain why Nicole chose to be female before she could have had any environmental or psychosocial influence.

In the medical world, epigenetics could potentially help understand many disorders that seemingly occur by “nature.”

[To be continued.]

Emotions versus Logic












