Sci is at Sci Am Blogs today, talking about deep brain stimulation as a treatment for depression, where they stimulate, and whether it’s a miracle cure, or just another method of treatment. Head over and check it out!
There’s a story that’s been flying around the internet (I saw the first bits this morning), that a group of scientists have found changes in brain activity associated with hyposexual desire disorder. Dr Petra and Maria Wolters and I got to chatting about it on Twitter, and wanting to find out what to REALLY think, we all went in search of the paper.
And this is where I got something that got my goat SO BAD.
The paper ISN’T OUT YET. The paper ISN’T WRITTEN YET. THERE IS NO PAPER. What there is, as far as I can tell, is an abstract presented at a very recent meeting.
I’m sure everyone here has heard of self-inflicted harm, or self-injurious behavior. The common word for it is “cutting”, and professionals and parents often worry about its presence in adolescent populations. But the population in which self-injurious behavior is most prevalent is actually in patients (adult or adolescent) with borderline personality disorder.
Borderline personality disorder (for some reason I wrote this up the first time as bipolar, but it’s IN THE TITLE. How tired am I. I blame Mr. S) is a disturbance in personality disorder which goes back and forth between self blame and blame of others, and which almost always include both severe emotional highs and severe emotional lows. The jury is still out on how exactly this works and what’s going on in the neural circuitry of people with BPD, but right now what we know is that they appear to have a lot of trouble regulating their emotions.
Yeah, duh, you might say. But it’s not as simple as just telling someone to calm down. What appears to be going on in BPD patients is that they have an overfunctioning of the limbic system of the brain, which is a group of brain areas associated with things like fear, emotion, and other behaviors. So if you have an overfunctioning in these areas, you might expect greater emotional highs and lows.
But the limbic system is restrained in part by input from the prefrontal cortex, that big area in the front of your brain which is devoted to what we like to call “higher function”, and which is often responsible for inhibiting impulsive behaviors and emotions. People with BPD ALSO have a dysfunction in THIS area, in particular what appears to be a hypofunctional system. So this means they are getting too much emotion from the limbic system, and too little reigning in from the prefrontal cortex. The result is a very dysregulated emotional state, with really high highs, and very low lows.
And one of the ways that people with BPD often attempt to deal with their excess emotion is through self-injurious behavior. Why is that?
This is post 5 in my ongoing, now-approaching-behemoth-size series of posts on depression. I’ve got other posts available on the etiology of depression, the current pharmacotherapies, studying depression in the lab, and the serotonin theory of depression, which of course you can read and refer to if you’re curious.
This post will be on what we currently know about the genetics of depression, the latest candidate genes, and what it means when scientists talk about genetic vulnerabilities and predisposition for disorders such as depression and bipolar disorder.
Yeah, today’s a big day, there’s a LOT I’ve written on depression, but do not fret, we will get through it all!!!
You can’t get through a whole day on depression without talking about some serotonin a little!
Hang on to your hats:
Oh yeah, she went there. Photo courtesy of The Loom blog from Discover. Sci might have to get one of these…
To begin with, I will admit that I do not know everything there is to know about serotonin. I am able to readily admit this because NO ONE knows everything there is to know about serotonin. This is not just because we haven’t figured it all out yet, but also because the serotonin system is completely, insanely complicated. You perform a pubmed search for “serotonin system review” and you get 176 PAGES of citations, all of them on things like “the serotonin system and anxiety”, “the serotonin system and cardiovascular effects”, “the serotonin system and gastrointestinal effects”, and the list goes on. To do a complete review of all that is currently known about the serotonin system would take hundreds of pages and probably thousands of citations. This is partially because serotonin not only does tons of things, but it does lots of stuff that has very little relation to any of the other stuff that is also doing. You can’t really make any sweeping generalizations about serotonin, there are always exceptions to the rule.
So what I’m going to go into here will be what I know about serotonin, as general as I can make it, and not covering even a quarter of what there is out there. But it will hopefully give you an idea of what people are talking about when they talk about serotonin drugs, serotonin effects, etc.
So here we go.
Welcome to depression post three, part of Back to Basics week at Neurotic Physiology!
Previously I covered the symptoms and etiology of depression, and some of the most common antidepressant medications and how they work. Now I’d like to go into some of the research behind it. After all, it’s not like we just grab a depressed person and say “here, take this and call me in the morning”. Every new drug that comes out on the market has to go through rigorous clinical testing to determine whether or not it works, and just as important, whether or not it is safe. And even then, drug companies and the FDA make mistakes.
This post (to save me writing another 2,000 words at a time) is going to focus on the way we study depression (along with other psychiatric disorders) using animal behavioral models, particularly rodent models. But of course, you can’t put a mouse on a couch and ask it how it feels about its mother. What researchers have found is that there are ways of studying the efficacy of traditional antidepressants. So rodent tests for depression are not so much tests for depression so much as they are screening for possible antidepressant therapies.
I’m sure that most people know that anorexia occurs more often in women than in men, though overall in about 0.3-0.6% of the population. What a lot of people DON’T know is that anorexia nervosa is a highly heritable disease. In fact, cases of anorexia nervosa have been reported as early as the 16th century or even earlier, long before being incredibly thin became a fashionable norm, which has led to the idea of anorexia as being a disorder that is more far-reaching than a desire to be thin.
Anorexia is characterized by severe weight loss or failure to gain weight when you’re supposed to, and is accompanied by intense fear of gaining weight, as well as body image distortion, usually believing that your body is far fatter than it actually is. Severe weight loss like this can lead to heart problems, and of course anorexia is also associated with other psychiatric disorders such as depression and anxiety, so people with anorexia have a high suicide rate as well.
Anorexia itself is actually divided into the traditional anorexia that we think of, which is the food restricting type, and the binge purge type of anorexia, which we usually call bulimia. Scientists now believe that they are two different symptoms of a similar disorder, and some scientists also consider aspects of anorexia to be highly similar to obsessive/compulsive disorder.
The question is, though, what makes anorexia heritable? What kind of genetic changes result in someone wanting to drastically restrict or control their food intake?
What if it had to do with estrogen?
*I did consider titling this “does this estrogen make me look fat”, but this is a rather serious subject and I threw that one out.
Let it be known that Sci, like many a young, bright-eyed little scientist, tries to keep up on her reading. TRIES is the operative word, but every week Sci gets the Tables of Contents for all the major journals in her field (and all the major ones in her subdisciple) emailed straight to her for her perusal. She scans the title lists, searching for things that are cool in her field, cool to blog, or that might indicate a scoopage of her work (hey, it happens).
And it was in one of these perusals that I came across this article. And this article is on a subject that needs to be blogged. But this article also says a lot about the “selling” of a scientific paper to a high-ranking journal. Biological Psychiatry, the journal in which this paper was published, has a pretty decent impact factor (8.67), and in Sci’s field, is considered to be a pretty hot publication venue.
But before I go into that, let’s take a look at this paper:
Steiner et al. “Fluoxetine potentiates methylphenidate-induced gene regulation in addiction-related brain regions: Concerns for use of cognitive enhancers?” Biological Psychiatry, 2010.
Sci would like to start by noting that doing an image search for “cognitive enhancer” yields some surprisingly boring results. I was really hoping for something like this:
Today’s post comes to you from several tweets that Sci received way back in the mists of time (that is…two weeks ago. Three? Something like that). Sci got wind of this paper and has been meaning to blog it for a while, but other things get in the way, like other things will. And when those other things finally get out of the way, Sci sometimes finds that she’s so SLEEPY she doesn’t know if she can make it through any more dry, sciency prose (sciency prose, even at the best of times, is pathetically dry. It’s why Sci blogs for you. See how she cares).
Like right now, when Sci is SO SLEEPY she just wants to lie down next to the cat and sack out. Scicat is currently reclining in a truly relaxed manner on the floor and isn’t making this any easier. But for the sake of stress, anxiety, depression, and a large glad of iced Moroccan mint green tea, SCI BLOGS ON.
(Sci’s determination very much resembles that of the bottom biting bug pictured here. A friend of mine showed this to me about a year ago, and it may still remain the oddest thing I have ever seen on the internet. Sci also finds it hilarious that every time anyone in Japan apparently trains for ANYTHING, they must at some point sit under a waterfall, and always end by looking determined on the top of Mt. Fuji. It’s like the Rocky Steps of Japan.)
Magalhaes, et al. “CRF receptor 1 regulates anxiety behavior via sensitization of 5-HT2 receptor signaling” Nature Neuroscience, 2010.