An unconventional treatment for depression: Sleep deprivation

I watched a good ‘psychological thriller’ the other night – Side Effects by Steven Soderbergh – that centers on a woman’s debilitating depression and critiques the pharmaceutical industry’s untoward influence over clinicians (it turns into a plot-twisty crime thriller, but that’s beside the point). The film got me thinking about our reliance on psychotropic medications to treat psychological distress, and how helpless we are when these pills don’t work.

I’ve written before on the over-medicalization of psychiatric disorders and the pharmaceutical industry’s role in this controversy, but this time the topic got me thinking about possible alternative treatments for depression, other than cognitive-behavioral therapy or mood-altering medications.

One innovative method for treating depression that has received attention is sleep deprivation. Acute sleep deprivation has been touted as having a 60% success rate in immediate relief from depression; however, this effect is temporary, only lasting until you finally do nod off.

At first this might seem surprising, after all, think about how cranky and irritable you feel after a poor night of sleep. But complete deprivation (i.e. missing an entire night’s sleep, or more than 12 hours) can actually have the opposite effect. Remember that loopy, giggly, hysterical feeling you used to get staying up all night at a sleepover, or at 5am in the library while studying for exams? It is believed that this phenomenon is at least partially caused by an alteration in activation and connectivity in our frontal cortex, potentially offsetting the harmful effects chronic depression can have on this area.

It is still relatively unknown how or why exactly this works though. A recent study from Tuft’s University attempted to answer this question by testing sleep deprivation and its efficacy as an anti-depressant in depressed mice. First, researchers confirmed that depressed animals who were sleep-deprived for 12 hours displayed significantly less depressive symptoms than control depressed mice. Then, for the first time, they were able to link this effect to the activation of a certain type of brain cell, astrocytes, that release a particular protein, adenosine.

Adenosine is important in sleep regulation, and its absence has also been implicated in a greater risk for depression. Adenosine release is increased the longer you’re awake (to a point), making you feel less aroused and more tired, and acting as part of your normal sleep-wake cycle. A beneficial side effect of its release now also appears to be an alleviation of depressive symptoms. However, after 72 hours of sleep deprivation there was no change in adenosine levels, as the astrocyte cells had largely shut down by this point. Thus, there was no effect of more extreme sleep deprivation on feelings of depression. Also, as soon as you do catch up on some zzz’s your adenosine levels return to normal and the anti-depressant effects disappear.

Adenosine’s effect on depression potentially works by altering the electrical signals in your brain, causing an immediate change in mood and behavior. Other fast-acting, unconventional treatments for depression, like deep brain stimulation and electro-shock therapy, are thought to work in a similar manner, impacting the brain’s electrical currents. These treatments also last much longer, suggesting that there may be a way to channel adenosine’s electrical effect into a longer-term solution.

I should be clear that I am in no way against using psychotropic medication to treat psychiatric disorders; in fact, in many instances these pills are absolutely essential. But in cases where these medications don’t work, or where their Side Effects are too severe (seriously, go see the movie!), it is important to have well-researched alternatives to the standard course of treatment. Also, it’s always nice to know how to get a good natural high every now and then, if you can stay up that long.

(Originally posted on Mind Read)

Pathologizing the norm: Follow-up

For those of you who are interested in this debate, there’s a great new two-part article in the New York Review of Books by Marcia Angell questioning “The Epidemic of Mental Illness.” The articles summarize three new books that are concerned about the prescription frenzy we are in the midst of and how this reliance on psychoactive medication came to be. She addresses the problem of dealing with psychiatric disorders as chemical imbalances and the dubious efficacy these drugs have in actually improving symptoms.

I highly recommend this read, as well as the second part in the series on “The Illusions of Psychiatry” for anyone concerned about our mental health system. One of the most resounding points she makes in the second piece is the perpetual expansion of the diagnoses listed in the American Psychological Association’s Diagnostics and Statistical Manual (DSM). With every publication of the DSM, there are more and more behaviors we have pathologized and “disorders” we have created, and with the upcoming publication of the DSM-V, there will certainly be a slew of new problems that we can put a name to and claim for ourselves. Angell succinctly describes this problem, stating, “Unlike the conditions treated in most other branches of medicine, there are no objective signs or tests for mental illness—no lab data or MRI findings—and the boundaries between normal and abnormal are often unclear. That makes it possible to expand diagnostic boundaries or even create new diagnoses, in ways that would be impossible, say, in a field like cardiology.”

Finally, she brings to task the drug companies who are more involved in psychiatric treatment than in any other medical field. This applies not only to clinicians and psychiatrists with private practices, but also the research institutions, hospitals, universities, policy makers, patient advocacy groups, educational organizations, and the APA itself.

Angell’s writing takes a good, hard look at the system of mental health, and while at times she makes some uncomfortable points, they are important issues that need to be addressed.

(Thanks to Emily Barnet for the Angell articles.)

The fascinating perils of plastic surgery

Cosmetic surgery and striving towards perfection of the body are nothing new. The first plastic surgery techniques date back to 800 BC in India, and there are records of ancient Egyptians and Romans carrying out reconstructive procedures. Karl Ferdinand Graefe first coined the phrase “rhinoplasty” in 1818 in an attempt to de-stigmatize nasal reconstructive surgery, and there was a resurgence of plastic surgery research and development after the first and second world wars in the U.S. and Britain. In more recent history, silicone breast enhancements emerged in the 1960s, and the economic boom in the 1980s, coupled with a flurry of modern-day developments in liposuction procedures, saw a rise in shrinking waists and thighs. Nowadays, surgical enhancements have been featured so often on reality TV and the cover of Playboy that we wouldn’t dream of considering them shocking. Yet there is still debate surrounding these procedures, and two new studies have come out recently reporting on the side effects and efficacy of plastic surgery. One study explores the implications on the brain, while the other investigates the long-term impact on the body.

study on the cognitive-emotional effects of Botox from my own alma mater, USC, looks not at the physical consequences of undergoing the needle, but at Botox’s effect on interpersonal relationships and empathy.

Body language and facial expressions are a large factor in interpersonal communications, almost as important as language itself. Humans are typically very good at relating to one another by subtly and subconsciously mirroring posture and facial expressions during the course of a conversation. This helps both parties to better perceive what is being expressed and what the appropriate response is. By mimicking a partner’s appearance, you are able to internalize their emotion, as your brain perceives your new expression and interprets the correct sentiment associated with it. When a friend is crying, you know they are upset and adopt their down-turned mouth and furrowed brow to better relate and express your empathy. Alternatively, when someone smiles at you on the street, it is difficult to not smile back and feel an extra bounce in your step. This phenomenon is known as “embodied cognition” and involves the reciprocal relationship between the brain and the body.

However, the USC scientists posit that by paralyzing your facial nerves, Botox (or botulinum toxin) disrupts this process by preventing your face from creating the creases and crinkles that externally express and internally manifest as emotions. The rest of the world may not be able to tell your age or know about that summer you spent in Greece, but it also won’t know that you’re empathizing with them when they tell you that their dog died.

The researchers tested this theory by injecting participants with Botox or a placebo dermal filler and having them perform a common test of empathy. Individuals were shown a picture of a set of eyes and asked to guess the emotion that best matched the ocular expression. Participants who received the Botox injection performed significantly worse on this task than controls, though they were still able to perform with around 70% accuracy.

Study author Dr. David Neal eloquently summarized the results, saying, “When you mimic you get a window into their inner world. When we can’t mimic, as with Botox, that window is a little darker.”

The second study involves the long-term physical effects of liposuction, questioning its enduring efficacy. Long heralded as a quick and relatively noninvasive fix for targeting fat areas, a recent study published in Obesity by researchers at the University of Colorado brings this notion into question. Drs. Teri Hernandez and Robert Eckel reported that people who received liposuction as part of the study had their body fat percentage return to baseline levels within one year of the procedure, as determined by subcutaneous skinfold thickness and MRI scans. However, the suctioned fat did not return to the areas that it was removed from; instead the regenerated fat was redistributed to areas less typically associated with fat storage, such as the upper abdomen and arms.

Scientists think that the gross number of fat cells in your body remains relatively stable throughout your life, determined in infancy and largely dependent on genetics and early diet. Instead, differences in weight gain or loss are typically seen through the size or fullness of the fat cells. These cells also exist in a relatively stable regional proportion throughout the body, relegating where an individual tends to gain or hold weight. However, after liposuction, the remaining tissue from the targeted areas are too traumatized to generate new cells, yet the body still attempts to maintain the balance of its original number. Therefore, new fat cells return after you’ve deleted them, just not in the areas you would expect.

Despite this news, more than half of the control subjects in the study–women who were initially interested in receiving liposuction but agreed to hold off for a year to serve as study controls–still wanted to undergo the procedure.

(Thanks to Ryan Essex for the article on Botox.)