Coping with the Winter Blues

I was recently interviewed for an article on coping with the “Winter Blues” in the Daily Muse, an online magazine.

This brief article offers some pithy guidance on what to do about seasonal depression. Check it out!

4 Ways to Cope with the Winter Blues

Is K Okay? Using Ketamine to Treat Depression

There have been some articles on the National Public Radio (NPR) website about the use of the drug ketamine as a fast acting treatment for depression (See here and here). Originally developed as an anesthetic, ketamine is better known to the public as the club drug Special K. Beginning with a study published in 2006 from a group of researchers with the National Institute of Health (NIH), ketamine has been explored as possible treatment for depression, and researchers are currently looking for chemically similar alternatives to ketamine with less potential for abuse.

A shortcoming for current antidepressants such as a Prozac is that it usually takes weeks to kick in, and even then, 30-40% of people don’t benefit. By contrast, studies suggest that intravenously-administered (IV) ketamine can improve mood in a matter of hours, and that change appears to last a week or two. For someone who is profoundly depressed and suicidal, this may be a useful alternative to inpatient hospitalization.

Ketamine targets a particular neurotransmitter — glutamate. Current antidepressants more commonly target serotonin, and often dopamine and/or norepinephrine, blocking their reuptake and increasing levels in the brain.

In one of the NPR articles, researcher Dr. Carlos Zarate compares depression to a “leaky faucet in the brain.” Current antidepressants, according to Dr. Zarate, “shut down the water plant,” which means that it a takes a long time for “water to stop flowing through the miles of pipes that eventually lead to the leaky faucet.” Ketamine, he suggests, stops the leaky faucet itself.

Although this metaphor is useful for making the distinction between a fast acting drug and one that takes longer to kick-in, it may also be misleading. The notion that a drug stops the “leaky faucet” of depression at the source sounds very precise and scientific. What may surprise some readers is that our understanding of the biology of depression is still pretty crude.

The Myth of the Chemical Imbalance

Once upon a time, psychiatry had a dream. The sudden introduction of antipsychotics and antidepressants in the 1950’s had a galvanizing effect on the field. It held out the possibility of developing medications that precisely targeted the biological causes of mental health problems.

Decades later, although providers still talk about antidepressants as restoring chemical imbalances, the evidence supporting this view has been pretty disappointing.

Earlier I mentioned that commonly prescribed antidepressants increase levels of some combination of the neurotransmitters serotonin, dopamine, and/or norepinephrine in the brain. As you might imagine, drug companies have poured millions into research to show that deficiencies in these neurotransmitters lead to depression—what is known as the Monoamine Hypothesis. Unfortunately, the research hasn’t found any compelling evidence these neurotransmitters cause depression—or at the very least the relationship between the two is not that simple.

For example, although not marketed in the US, there’s an antidepressant called tianeptine that decreases concentrations of serotonin in the brain. Research suggests it’s just as effective as antidepressants that increase concentrations in the brain. This is a bit of a conundrum for the chemical imbalance theory of depression.

Therefore, there’s not a lot of evidence to support the popular notion that antidepressants restore a chemical imbalance. Instead, it’s more accurate to say that antidepressants artificially increase levels of certain neurotransmitters in ways that some people find reduce feelings of depression and anxiety.

Fast Acting Drugs are Not Necessarily Better: The Case of Anxiety

Another thing that concerns me about ketamine is that fast acting drugs are not always a good thing. Case in point: antianxiety medications. No one particularly enjoys feeling anxious. We often want instant relief, or at least something to take the edge off. There’s a class of medications that do just that—benzodiazepines, which including some more commonly known drugs such as Xanax and Ativan. These drugs tend to work pretty quickly, often within 30 minutes.

Although they are commonly prescribed, the problem with benzodiazepines is that long-term use can lead to long-term problems. First of all, these medications pose a high risk of abuse, dependency, and, withdrawal problems. In addition, there is research to suggest that many people experience “rebound effects” once they stop taking these medications—that is, they find that their anxiety is even worse than when they started taking the medication. For these reasons, although many providers continue to prescribe benzodiazepines in the short-term, most experts would agree that antidepressant medications which also tend to blunt anxious feelings are a safer alternative in the long-term.

BTW: Did You Know Ketamine Intoxication Can Mimic Schizophrenia?

 Low doses of ketamine appear to reduce depression very quickly. But as the Neuroskeptic blog noted a few years ago, there’s also a strain of research that shows that high doses of ketamine can cause symptoms that mimic schizophrenia.

This finding in itself doesn’t mean the drug is bad. Medications for Parkinson’s disease, which increase dopamine, can also cause schizophrenia-like symptom. (Conversely, long-term use of antipsychotics can cause Parkinsonian-like symptoms in people with schizophrenia.) My point here is that, although researchers have found another potential treatment for depression, it’s unlikely they’ve uncovered the core biological root of depression.

Where Does That Leave Us?

For these reasons, I wince when I hear people talk of “miracle drugs” for psychological problems. It’s not that I see no future for ketamine in depression treatment. It’s more that I found the NPR articles overly optimistic.

As a scientist, I support the continued study of ketamine and related drugs as a potential treatment for depression; however, I’m skeptical about the breadth of its usefulness based on all the other times we’ve gone down this road of “miracle drug” cures. Consequently, although I think ketamine has the potential to be a genuinely new medical approach (i.e., not another minor tweak of an already prescribed antidepressant) to dealing with profound depression, I think we should temper our optimism a bit. The first study on the use of ketamine to treat depression was published in 2006, and the data of if, under what circumstances, and how this drug may be useful are still very much unknown.

It may be, for example, that researchers find ketamine can be useful for people who show up in Emergency Departments suicidally depressed. Rather than sending them to a locked ward, which costs over $1,000 a day, emergency physicians may give them an IV of ketamine. If they respond and mood improves, they can be given an appointment with an outpatient specialist that week and be sent home without further disruption to their lives.

Perhaps this is even how the NIH researchers have conceived of the drug—if so, it wasn’t conveyed in the NPR articles. It seems there is potential for ketamine to be useful in this kind of a scenario, but again, we just don’t have the data yet to know with any certainty. What concerns me is that, based on reports in the media like those on NPR suggesting a “miracle drug” or a “cure,” people may think “I’m depressed—I need some ketamine.” This is a dangerous path where short-term gains could lead to long-term consequences.

PLEASE NOTE: PORTLAND PSYCHOTHERAPY IS NOT INVOLVED IN KETAMINE TREATMENT.

There’ve been some articles on the National Public Radio (NPR) website about the use of the drug ketamine as a fast acting treatment for depression (See here and here). Originally developed as an anesthetic, ketamine is better known to the public as the club drug Special K. Beginning with a study published in 2006 from a group of researchers with the National Institute of Health (NIH), ketamine has been explored as possible treatment for depression, and researchers are currently looking for chemically similar alternatives to ketamine with less potential for abuse.

A shortcoming for current antidepressants such as a Prozac is that it usually takes weeks to kick in, and even then, 30-40% of people don’t benefit. By contrast, studies suggest that intravenously-administered (IV) ketamine can improve mood in a matter of hours, and that change appears to last a week or two. For someone who is profoundly depressed and suicidal, this may be a useful alternative to inpatient hospitalization.

Ketamine targets a particular neurotransmitter glutamate. Current antidepressants more commonly target serotonin, and often dopamine and/or norepinephrine, blocking their reuptake and increasing levels in the brain.

In one of the NPR articles, researcher Dr. Carlos Zarate compares depression to a “leaky faucet in the brain.” Current antidepressants, according to Dr. Zarate, “shut down the water plant,” which means that it a takes a long time for “water to stop flowing through the miles of pipes that eventually lead to the leaky faucet.” Ketamine, he suggests, stops the leaky faucet itself.

Although this metaphor is useful for making the distinction between a fast acting drug and one that takes longer to kick-in, it may also be misleading. The notion that a drug stops the “leaky faucet” of depression at the source sounds very precise and scientific. What may surprise some readers is that our understanding of the biology of depression is still pretty crude.

The Myth of the Chemical Imbalance

Once upon a time, psychiatry had a dream. The sudden introduction of antipsychotics and antidepressants in the 1950’s had a galvanizing effect on the field. It held out the possibility of developing medications that precisely targeted the biological causes of mental health problems.

Decades later, although providers still talk about antidepressants as restoring chemical imbalances, the evidence supporting this view has been pretty disappointing.

Earlier I mentioned that commonly prescribed antidepressants increase levels of some combination of the neurotransmitters serotonin, dopamine, and/or norepinephrine in the brain. As you might imagine, drug companies have poured millions into research to show that deficiencies in these neurotransmitters lead to depression—what is known as the Monoamine Hypothesis. Unfortunately, the research hasn’t found any compelling evidence these neurotransmitters cause depression—or at the very least the relationship between the two is not that simple.

For example, although not marketed in the US, there’s an antidepressant called tianeptine that decreases concentrations of serotonin in the brain. Research suggests it’s just as effective as antidepressants that increase concentrations in the brain. This is a bit of a conundrum for the chemical imbalance theory of depression.

Therefore, there’s not a lot of evidence to support the popular notion that antidepressants restore a chemical imbalance. Instead, it’s more accurate to say that antidepressants artificially increase levels of certain neurotransmitters in ways that some people find reduce feelings of depression and anxiety.

Fast Acting Drugs are Not Necessarily Better: The Case of Anxiety

Another thing that concerns me about ketamine is that fast acting drugs are not always a good thing. Case in point: antianxiety medications. No one particularly enjoys feeling anxious. We often want instant relief, or at least something to take the edge off. There’s a class of medications that do just that—benzodiazepines, which including some more commonly known drugs such as Xanax and Ativan. These drugs tend to work pretty quickly, often within 30 minutes.

Although they are commonly prescribed, the problem with benzodiazepines is that long-term use can lead to long-term problems. First of all, these medications pose a high risk of abuse, dependency, and, withdrawal problems. In addition, there is research to suggest that many people experience “rebound effects” once they stop taking these medications—that is, they find that their anxiety is even worse than when they started taking the medication. For these reasons, although many providers continue to prescribe benzodiazepines in the short-term, most experts would agree that antidepressant medications which also tend to blunt anxious feelings are a safer alternative in the long-term.

BTW: Did You Know Ketamine Intoxication Can Mimic Schizophrenia?

 Low doses of ketamine appear to reduce depression very quickly. But as the Neuroskeptic blog noted a few years ago, there’s also a strain of research that shows that high doses of ketamine can cause symptoms that mimic schizophrenia.

This finding in itself doesn’t mean the drug is bad. Medications for Parkinson’s disease, which increase dopamine, can also cause schizophrenia-like symptom. (Conversely, long-term use of antipsychotics can cause Parkinsonian-like symptoms in people with schizophrenia.) My point here is that, although researchers have found another potential treatment for depression, it’s unlikely they’ve uncovered the core biological root of depression.

Where Does That Leave Us?

For these reasons, I wince when I hear people talk of “miracle drugs” for psychological problems. It’s not that I see no future for ketamine in depression treatment. It’s more that I found the NPR articles overly optimistic.

As a scientist, I support the continued study of ketamine and related drugs as a potential treatment for depression; however, I’m skeptical about the breadth of its usefulness based on all the other times we’ve gone down this road of “miracle drug” cures. Consequently, although I think ketamine has the potential to be a genuinely new medical approach (i.e., not another minor tweak of an already prescribed antidepressant) to dealing with profound depression, I think we should temper our optimism a bit. The first study on the use of ketamine to treat depression was published in 2006, and the data of if, under what circumstances, and how this drug may be useful are still very much unknown.

It may be, for example, that researchers find ketamine can be useful for people who show up in Emergency Departments suicidally depressed. Rather than sending them to a locked ward, which costs over $1,000 a day, emergency physicians may give them an IV of ketamine. If they respond and mood improves, they can be given an appointment with an outpatient specialist that week and be sent home without further disruption to their lives.

Perhaps this is even how the NIH researchers have conceived of the drug—if so, it wasn’t conveyed in the NPR articles. It seems there is potential for ketamine to be useful in this kind of a scenario, but again, we just don’t have the data yet to know with any certainty. What concerns me is that, based on reports in the media like those on NPR suggesting a “miracle drug” or a “cure,” people may think “I’m depressed—I need some ketamine.” This is a dangerous path where short-term gains could lead to long-term consequences.

 

Can Light in the Ears Cure the Winter Blues or Do You Need a Hole in Your Head?

Here in Portland, seasonal depression, commonly called the Winter Blues or Seasonal Affective Disorder, is relatively common. Up to 20% of the population in the rainy Pacific Northwest may be impacted. I’ve written more extensively in another blog about the Winter Blues and how light boxes are an effective treatment.

It’s not available in the U.S. yet, but a Finnish company is marketing a new device called “Valkee.” It looks like an iPod, except instead of digital music, the headphones shine light into your ear. Yes, that’s right, the Valkee has small ear buds that shine light into your ear.

Why would shining bright light in your ear help with seasonal depression? Here’s where things turn a little fuzzy.

Why Light Boxes Work

Perhaps we might start with light boxes, the treatment with the greatest research support for the Winter Blues. With light box therapy, people sit in front of specially-designed devices that give off light at a specific intensity or lux—10,000 lux is optimal for bright spectrum white light boxes.

Light serves as a signal to our brain that it’s daytime. The accepted pathway is through our eyes. When light hits our retina, it sends signal to our brains; specifically, the signals travel to an area called the suprachiasmatic nucleus (SCN). This area controls our circadian rhythms or internal clock.

The shorter days and dark mornings of the fall and winter months, particularly in northern latitudes such as Portland, can lead to a desynchronization between our internal clock and our actual day. Light box therapy is a way to fix this. Regular use of a light box before dawn can signal to the brain that it’s time to get up and start our day, even though it’s dark and cloudy out.

Here we have a well-researched pathway and mechanism of action: daylight in our eyes signals to the brain that it’s time to get up, cueing up our circadian rhythms (aka our internal clock). Why would shining a light in our ears be a more effective pathway? This is unclear to me. It’s not as if we spend our summers tilting our heads so that the sunlight can stream into our ears.

But Valkee Makes Some Pretty Unlikely Claims

The company cites results from research studies that suggest their device has some very impressive outcomes. Perhaps a bit too impressive. For example, one article claims that “92% of people with SAD achieved full remission” from depression. If you’re familiar with depression research, a 92% response—particularly with “full remission”—is an incredible claim. As a point of comparison, with light box therapy, the most well established treatment, about 60-70% of people respond—and here we’re talking about decreases in depressive symptoms, not necessarily full remission.

Let’s Take a Look at Valkee’s Research

The Valkee website has a tab for “Evidence,” listing research studies. If the device is as incredibly effective as the company suggests, you might expect to find citations in high-ranking peer-reviewed journals where other researcher could look over the results and study them. Respected scientific journals serve as a gateway for quality research.

Instead, the only citations for the device are from conference poster presentations. Curiously, the poster presentations are all from 2011. There’s nothing wrong with poster presentations, but you don’t need a high quality study for a conference to accept a poster presentation. In fact, it’s not uncommon for people to present posters at conferences for studies that they haven’t yet conducted (as a way to get feedback).

[UPDATE 03/2014: Someone at Valkee has since pointed out since I wrote my orginal post a few years ago that they have expanded the research section on their website. The research does not alter my overall opinion, but I wanted to note that there are more studies listed. ]

[UPDATE 9/2014: We have written another article on the Valkee in light of new information on the device since this article was written]

Normally with any scientific treatment, there is a period of testing and refinement before it’s made available to the public. With the Valkee, we have a slick-looking device that was released before any research has been published.

Should I Buy a Valkee?

From what I’ve seen, I’d hold off on exchanging your hard-earned dollars for euros and plunking down your hard-earned money (£185 or $240) for a Valkee. (It’s not available in the US yet.) The plausibility for the why it works is unclear, and the research supporting its effectiveness is very limited. I could wrong—perhaps future research will show that shining light in your ears is a more effective treatment for the Winter Blues than light boxes. However, the Valkee may be little more than an expensive flashlight. And it doesn’t even play MP3’s.

Archives by Month