Tonight I got to go with my Nono. He was doing some recording at the studio. He got to do his singing tonight. It was so much fun to watch him work! And he has such a beautiful voice. :)
His group is recording a new CD. And it was really neat to watch them put it together. I'm glad I got to go. They even let my Nono and I record a song together. I know it wasn't as professional as the stuff they are working on. But it was fun.
And now I have a CD of my Nono and me singing! It's really special. I'm glad the other guys were there too. Because they did all the music. I had a lot of fun! I'm so glad we got to come. I'll never forget tonight. :) C
Wednesday, December 30, 2009
Tuesday, December 29, 2009
ECT in Nixonland
I've just finished Nixonland, Rick Perlstein's history of the 1960s. Some things I learned: Richard Nixon was a genius, albeit an evil one; the 1960s never ended; Rick Perlstein is my new favourite political author.The book also reminded me of a sad episode in the history of psychiatry.
George McGovern ran against Nixon as the Democratic candidate for President in 1972. He was essentially the Obama of the 60s generation: unashamedly liberal and intellectual, he unseated the "established" candidate, Hubert Humphrey, to clinch the Democrat's nomination after a bitter primary campaign thanks to his idealistic young grass-roots.
McGovern had difficulty choosing his vice-presidential running mate, and eventually chose a little-known Senator from Missouri, Thomas Eagleton (left in the photo). It seemed a safe enough choice. Until Eagleton's first press conference.
Eagleton revealed that he'd been treated in a psychiatric hospital for "exhaustion" - everyone knew he meant clinical depression - three times, and that he had received electroconvulsive therapy twice. McGovern hadn't known this when he picked him.
From there it was all downhill. McGovern initially said he backed Eagleton "1000%". But to some, the idea of putting someone who'd had shock therapy a heartbeat away from the Presidency was unacceptable, and after two weeks of gossip, McGovern dropped him from the ticket.
Perlstein notes that this move wrecked McGovern's image as the idealistic and authentic alternative to politics-as-usual. Polls showed that Americans overwhelmingly trusted Nixon over McGovern, even as the facts about Watergate were emerging. Nixon won a landslide.
ECT in Nixonland
I've just finished Nixonland, Rick Perlstein's history of the 1960s. Some things I learned: Richard Nixon was a genius, albeit an evil one; the 1960s never ended; Rick Perlstein is my new favourite political author.The book also reminded me of a sad episode in the history of psychiatry.
George McGovern ran against Nixon as the Democratic candidate for President in 1972. He was essentially the Obama of the 60s generation: unashamedly liberal and intellectual, he unseated the "established" candidate, Hubert Humphrey, to clinch the Democrat's nomination after a bitter primary campaign thanks to his idealistic young grass-roots.
McGovern had difficulty choosing his vice-presidential running mate, and eventually chose a little-known Senator from Missouri, Thomas Eagleton (left in the photo). It seemed a safe enough choice. Until Eagleton's first press conference.
Eagleton revealed that he'd been treated in a psychiatric hospital for "exhaustion" - everyone knew he meant clinical depression - three times, and that he had received electroconvulsive therapy twice. McGovern hadn't known this when he picked him.
From there it was all downhill. McGovern initially said he backed Eagleton "1000%". But to some, the idea of putting someone who'd had shock therapy a heartbeat away from the Presidency was unacceptable, and after two weeks of gossip, McGovern dropped him from the ticket.
Perlstein notes that this move wrecked McGovern's image as the idealistic and authentic alternative to politics-as-usual. Polls showed that Americans overwhelmingly trusted Nixon over McGovern, even as the facts about Watergate were emerging. Nixon won a landslide.
Sunday, December 27, 2009
The Genetics of Living To 100
Is there a gene for long life?
Boston-based group Sebastiani et al say they've found not one but two, in RNA Editing Genes Associated with Extreme Old Age in Humans and with Lifespan in C. elegans.
They took 4 groups of "oldest old" people: from New England, Italy, and Japan, and American Ashkenazi Jews. All were aged 90 or more, and many of them were 100, centenarians. As control groups, they used random healthy people who weren't especially old. The total sample size was an impressive 2105 old vs. 3044 controls.
On the basis of a pilot study, they chose to look at two candidate genes, ADARB1 and ADARB2. Both are involved in post-transcriptional RNA editing, one of the steps in the process by which genetic material, DNA, controls protein synthesis. It's something every cell in the body needs to do in order to function.
What happened? Their abstract makes the exciting claim that
In ADARB2, out of 114 variants, 10 were significantly associated in the New England sample. Of these, 4 were independently significant in the Italian sample, and in the combined New England/Italian sample all 10 were still associated. But the Jewish and the Japanese samples showed a rather different picture: only 1 of the 10 associations was significant in the Jews, although several were weakly associated in the same direction, and in a pooled New England/Italian/Jewish analysis 9 were still significant. In the Japanese sample, one association was replicated but another variant was associated in the wrong direction.
They also did some lab work and found that in nematode worms (C. Elegans), mutants lacking the worm equivalent of the ADARB1 and ADARB2 genes had a 50% reduced lifespan - 10 days, instead of the normal 20 - despite no obvious symptoms of illness. Hmm.
I'm not quite sure what to make of this data. They looked at 4 separate, large samples, which is an excellent size by the standards of candidate gene association studies. The evidence implicating ADARB1 and (especially) ADARB2 variants in longevity is fairly convincing, although the most consistent effects came from the European-ancestry samples, suggesting that different things might be going on in other populations. This is the first research looking at these genes; ultimately, we won't know for sure until we get more. The worm data is a nice touch, but I'd like to see evidence from animals with a bit more similarity to humans, say mice.
Still, suppose that these genes are associated with long life; suppose they they control the rate of the ageing process, protecting you from dying from "natural causes" too early. That doesn't mean that you'll live to an old age - it just makes it possible. If you get hit a truck or fall of a cliff, you're dead, anti-ageing genes or not.
Frenchwoman Jeanne Calment, born 1875, died 1997, is the oldest person on record, at 122 years. But we'll never know whether someone with the genetic potential to outlive her died in WW2, or the Cultural Revolution, or just got hit by a truck. Calment presumably had the right genes, but she was also lucky.
So a trait's being genetically heritable doesn't make it pre-ordained and immutable. IQ, for example, most likely has a heritability of around 50% - some people likely have a higher potential for intellectual achievement than others. But if you're born into an abusive family, or deep poverty, or you never get a chance to go to school, you may never reach that potential. There's always that truck.
Sebastiani P, Montano M, Puca A, Solovieff N, Kojima T, Wang MC, Melista E, Meltzer M, Fischer SE, Andersen S, Hartley SH, Sedgewick A, Arai Y, Bergman A, Barzilai N, Terry DF, Riva A, Anselmi CV, Malovini A, Kitamoto A, Sawabe M, Arai T, Gondo Y, Steinberg MH, Hirose N, Atzmon G, Ruvkun G, Baldwin CT, & Perls TT (2009). RNA editing genes associated with extreme old age in humans and with lifespan in C. elegans. PloS one, 4 (12) PMID: 20011587
Boston-based group Sebastiani et al say they've found not one but two, in RNA Editing Genes Associated with Extreme Old Age in Humans and with Lifespan in C. elegans.They took 4 groups of "oldest old" people: from New England, Italy, and Japan, and American Ashkenazi Jews. All were aged 90 or more, and many of them were 100, centenarians. As control groups, they used random healthy people who weren't especially old. The total sample size was an impressive 2105 old vs. 3044 controls.
On the basis of a pilot study, they chose to look at two candidate genes, ADARB1 and ADARB2. Both are involved in post-transcriptional RNA editing, one of the steps in the process by which genetic material, DNA, controls protein synthesis. It's something every cell in the body needs to do in order to function.
What happened? Their abstract makes the exciting claim that
18 single nucleotide polymorphisms (SNPs) in the RNA editing genes ADARB1 and ADARB2 are associated with extreme old age in a U.S. based study ... We describe replications of these findings in three independently conducted centenarian studies with different genetic backgrounds (Italian, Ashkenazi Jewish and Japanese) that collectively support an association of ADARB1 and ADARB2 with longevity.But read the whole paper and the picture is a little more complex. For ADARB1, they looked at 31 variants (SNPs). In the New England sample, which was the largest, 5 of them were statistically significantly more common in old people compared to the controls. However, none of these were significantly associated in any of the other samples, although for 3 of the 5 variants, there was some evidence of an effect in the same direction in the other samples.
In ADARB2, out of 114 variants, 10 were significantly associated in the New England sample. Of these, 4 were independently significant in the Italian sample, and in the combined New England/Italian sample all 10 were still associated. But the Jewish and the Japanese samples showed a rather different picture: only 1 of the 10 associations was significant in the Jews, although several were weakly associated in the same direction, and in a pooled New England/Italian/Jewish analysis 9 were still significant. In the Japanese sample, one association was replicated but another variant was associated in the wrong direction.
They also did some lab work and found that in nematode worms (C. Elegans), mutants lacking the worm equivalent of the ADARB1 and ADARB2 genes had a 50% reduced lifespan - 10 days, instead of the normal 20 - despite no obvious symptoms of illness. Hmm.
I'm not quite sure what to make of this data. They looked at 4 separate, large samples, which is an excellent size by the standards of candidate gene association studies. The evidence implicating ADARB1 and (especially) ADARB2 variants in longevity is fairly convincing, although the most consistent effects came from the European-ancestry samples, suggesting that different things might be going on in other populations. This is the first research looking at these genes; ultimately, we won't know for sure until we get more. The worm data is a nice touch, but I'd like to see evidence from animals with a bit more similarity to humans, say mice.
Still, suppose that these genes are associated with long life; suppose they they control the rate of the ageing process, protecting you from dying from "natural causes" too early. That doesn't mean that you'll live to an old age - it just makes it possible. If you get hit a truck or fall of a cliff, you're dead, anti-ageing genes or not.
Frenchwoman Jeanne Calment, born 1875, died 1997, is the oldest person on record, at 122 years. But we'll never know whether someone with the genetic potential to outlive her died in WW2, or the Cultural Revolution, or just got hit by a truck. Calment presumably had the right genes, but she was also lucky.
So a trait's being genetically heritable doesn't make it pre-ordained and immutable. IQ, for example, most likely has a heritability of around 50% - some people likely have a higher potential for intellectual achievement than others. But if you're born into an abusive family, or deep poverty, or you never get a chance to go to school, you may never reach that potential. There's always that truck.
Sebastiani P, Montano M, Puca A, Solovieff N, Kojima T, Wang MC, Melista E, Meltzer M, Fischer SE, Andersen S, Hartley SH, Sedgewick A, Arai Y, Bergman A, Barzilai N, Terry DF, Riva A, Anselmi CV, Malovini A, Kitamoto A, Sawabe M, Arai T, Gondo Y, Steinberg MH, Hirose N, Atzmon G, Ruvkun G, Baldwin CT, & Perls TT (2009). RNA editing genes associated with extreme old age in humans and with lifespan in C. elegans. PloS one, 4 (12) PMID: 20011587
The Genetics of Living To 100
Is there a gene for long life?
Boston-based group Sebastiani et al say they've found not one but two, in RNA Editing Genes Associated with Extreme Old Age in Humans and with Lifespan in C. elegans.
They took 4 groups of "oldest old" people: from New England, Italy, and Japan, and American Ashkenazi Jews. All were aged 90 or more, and many of them were 100, centenarians. As control groups, they used random healthy people who weren't especially old. The total sample size was an impressive 2105 old vs. 3044 controls.
On the basis of a pilot study, they chose to look at two candidate genes, ADARB1 and ADARB2. Both are involved in post-transcriptional RNA editing, one of the steps in the process by which genetic material, DNA, controls protein synthesis. It's something every cell in the body needs to do in order to function.
What happened? Their abstract makes the exciting claim that
In ADARB2, out of 114 variants, 10 were significantly associated in the New England sample. Of these, 4 were independently significant in the Italian sample, and in the combined New England/Italian sample all 10 were still associated. But the Jewish and the Japanese samples showed a rather different picture: only 1 of the 10 associations was significant in the Jews, although several were weakly associated in the same direction, and in a pooled New England/Italian/Jewish analysis 9 were still significant. In the Japanese sample, one association was replicated but another variant was associated in the wrong direction.
They also did some lab work and found that in nematode worms (C. Elegans), mutants lacking the worm equivalent of the ADARB1 and ADARB2 genes had a 50% reduced lifespan - 10 days, instead of the normal 20 - despite no obvious symptoms of illness. Hmm.
I'm not quite sure what to make of this data. They looked at 4 separate, large samples, which is an excellent size by the standards of candidate gene association studies. The evidence implicating ADARB1 and (especially) ADARB2 variants in longevity is fairly convincing, although the most consistent effects came from the European-ancestry samples, suggesting that different things might be going on in other populations. This is the first research looking at these genes; ultimately, we won't know for sure until we get more. The worm data is a nice touch, but I'd like to see evidence from animals with a bit more similarity to humans, say mice.
Still, suppose that these genes are associated with long life; suppose they they control the rate of the ageing process, protecting you from dying from "natural causes" too early. That doesn't mean that you'll live to an old age - it just makes it possible. If you get hit a truck or fall of a cliff, you're dead, anti-ageing genes or not.
Frenchwoman Jeanne Calment, born 1875, died 1997, is the oldest person on record, at 122 years. But we'll never know whether someone with the genetic potential to outlive her died in WW2, or the Cultural Revolution, or just got hit by a truck. Calment presumably had the right genes, but she was also lucky.
So a trait's being genetically heritable doesn't make it pre-ordained and immutable. IQ, for example, most likely has a heritability of around 50% - some people likely have a higher potential for intellectual achievement than others. But if you're born into an abusive family, or deep poverty, or you never get a chance to go to school, you may never reach that potential. There's always that truck.
Sebastiani P, Montano M, Puca A, Solovieff N, Kojima T, Wang MC, Melista E, Meltzer M, Fischer SE, Andersen S, Hartley SH, Sedgewick A, Arai Y, Bergman A, Barzilai N, Terry DF, Riva A, Anselmi CV, Malovini A, Kitamoto A, Sawabe M, Arai T, Gondo Y, Steinberg MH, Hirose N, Atzmon G, Ruvkun G, Baldwin CT, & Perls TT (2009). RNA editing genes associated with extreme old age in humans and with lifespan in C. elegans. PloS one, 4 (12) PMID: 20011587
Boston-based group Sebastiani et al say they've found not one but two, in RNA Editing Genes Associated with Extreme Old Age in Humans and with Lifespan in C. elegans.They took 4 groups of "oldest old" people: from New England, Italy, and Japan, and American Ashkenazi Jews. All were aged 90 or more, and many of them were 100, centenarians. As control groups, they used random healthy people who weren't especially old. The total sample size was an impressive 2105 old vs. 3044 controls.
On the basis of a pilot study, they chose to look at two candidate genes, ADARB1 and ADARB2. Both are involved in post-transcriptional RNA editing, one of the steps in the process by which genetic material, DNA, controls protein synthesis. It's something every cell in the body needs to do in order to function.
What happened? Their abstract makes the exciting claim that
18 single nucleotide polymorphisms (SNPs) in the RNA editing genes ADARB1 and ADARB2 are associated with extreme old age in a U.S. based study ... We describe replications of these findings in three independently conducted centenarian studies with different genetic backgrounds (Italian, Ashkenazi Jewish and Japanese) that collectively support an association of ADARB1 and ADARB2 with longevity.But read the whole paper and the picture is a little more complex. For ADARB1, they looked at 31 variants (SNPs). In the New England sample, which was the largest, 5 of them were statistically significantly more common in old people compared to the controls. However, none of these were significantly associated in any of the other samples, although for 3 of the 5 variants, there was some evidence of an effect in the same direction in the other samples.
In ADARB2, out of 114 variants, 10 were significantly associated in the New England sample. Of these, 4 were independently significant in the Italian sample, and in the combined New England/Italian sample all 10 were still associated. But the Jewish and the Japanese samples showed a rather different picture: only 1 of the 10 associations was significant in the Jews, although several were weakly associated in the same direction, and in a pooled New England/Italian/Jewish analysis 9 were still significant. In the Japanese sample, one association was replicated but another variant was associated in the wrong direction.
They also did some lab work and found that in nematode worms (C. Elegans), mutants lacking the worm equivalent of the ADARB1 and ADARB2 genes had a 50% reduced lifespan - 10 days, instead of the normal 20 - despite no obvious symptoms of illness. Hmm.
I'm not quite sure what to make of this data. They looked at 4 separate, large samples, which is an excellent size by the standards of candidate gene association studies. The evidence implicating ADARB1 and (especially) ADARB2 variants in longevity is fairly convincing, although the most consistent effects came from the European-ancestry samples, suggesting that different things might be going on in other populations. This is the first research looking at these genes; ultimately, we won't know for sure until we get more. The worm data is a nice touch, but I'd like to see evidence from animals with a bit more similarity to humans, say mice.
Still, suppose that these genes are associated with long life; suppose they they control the rate of the ageing process, protecting you from dying from "natural causes" too early. That doesn't mean that you'll live to an old age - it just makes it possible. If you get hit a truck or fall of a cliff, you're dead, anti-ageing genes or not.
Frenchwoman Jeanne Calment, born 1875, died 1997, is the oldest person on record, at 122 years. But we'll never know whether someone with the genetic potential to outlive her died in WW2, or the Cultural Revolution, or just got hit by a truck. Calment presumably had the right genes, but she was also lucky.
So a trait's being genetically heritable doesn't make it pre-ordained and immutable. IQ, for example, most likely has a heritability of around 50% - some people likely have a higher potential for intellectual achievement than others. But if you're born into an abusive family, or deep poverty, or you never get a chance to go to school, you may never reach that potential. There's always that truck.
Sebastiani P, Montano M, Puca A, Solovieff N, Kojima T, Wang MC, Melista E, Meltzer M, Fischer SE, Andersen S, Hartley SH, Sedgewick A, Arai Y, Bergman A, Barzilai N, Terry DF, Riva A, Anselmi CV, Malovini A, Kitamoto A, Sawabe M, Arai T, Gondo Y, Steinberg MH, Hirose N, Atzmon G, Ruvkun G, Baldwin CT, & Perls TT (2009). RNA editing genes associated with extreme old age in humans and with lifespan in C. elegans. PloS one, 4 (12) PMID: 20011587
Saturday, December 26, 2009
Being Lazy
We're being really lazy around here. But we need to pack our bags. Because we're going to go visit my Nono in Florida. We leave tomorrow. My abuelitas are really excited too!
My Nono already has our entire trip planned. And we get to spend New Year's Eve at Disney World. We're going for more than 1 day. But we get to spend that day there! It's going to be a lot of fun!
Now I just need to talk my Dad into packing his bags. We've been watching movies all day. And eating lots of yummy cookies! But we've got some work to do. Because we have to be at the airport tomorrow at 4 in the morning! :) C
My Nono already has our entire trip planned. And we get to spend New Year's Eve at Disney World. We're going for more than 1 day. But we get to spend that day there! It's going to be a lot of fun!
Now I just need to talk my Dad into packing his bags. We've been watching movies all day. And eating lots of yummy cookies! But we've got some work to do. Because we have to be at the airport tomorrow at 4 in the morning! :) C
The War on "Interesting"
My New Year's Blog Resolution - no more calling things "interesting".
While writing, I sometimes find myself searching for an adjective to attach to something I've just mentioned, words to explain why I think it's relevant. It's... no... it's kind of... hmm... It's interesting, is what it is! Phew. Now I can move on. Anything can be "interesting" - a book, a blog post, an article, an event, an idea, a movement, a prediction, an argument.
Calling something interesting is effortless; easy; it's a one-size-fits-all term. If you can't think of anything else to say, you can at least say that. Which is why people do. I know I'm not alone in this.
But "interesting" is a cop-out. It adds nothing. If you're taking the trouble of writing about something, it should be taken as read that you think it's interesting. The whole point is to explain why - to tell people what's special about it. Does it present new evidence? If so, is it reliable? Does it introduce a new distinction, a new vocabulary, a new way of thinking? If so, why is it a good one?
Sadly it's easier to just call something interesting than to explain why it is. Partly this is because "interesting" (or "fascinating", "thought-provoking", "intriguing", "notable" etc.) is just one word, and it's easier to write one word than a sentence. More important is the fact that you probably don't know why you're interested by something until you do some thinking about it.
Don't duck out of doing that thinking. It's intellectual laziness. Even more so is to say that you're not sure if something is true, but it sure is interesting. "It's not necessarily true, but it's a fascinating thought" - is it? why?
Are you interested by the possibility that it's true, so if you learned that it was definitely false, it would become boring? Or is it one of those ideas that's interesting "in itself"? If so, why? Because it's an influential idea in a political or historical sense? Because it sheds light on the minds of the people who believe it? Are you sure that your interest isn't a kind of repressed belief? Are you really "only interested", or do you see something you like? If so, why not say so?
So, I'm quitting the habit, cold turkey, as of now. No more will I reach for the "interesting" button whenever I'm stuck for words. With any luck, this will make my writing a little bit more interes... hmm.
While writing, I sometimes find myself searching for an adjective to attach to something I've just mentioned, words to explain why I think it's relevant. It's... no... it's kind of... hmm... It's interesting, is what it is! Phew. Now I can move on. Anything can be "interesting" - a book, a blog post, an article, an event, an idea, a movement, a prediction, an argument.Calling something interesting is effortless; easy; it's a one-size-fits-all term. If you can't think of anything else to say, you can at least say that. Which is why people do. I know I'm not alone in this.
But "interesting" is a cop-out. It adds nothing. If you're taking the trouble of writing about something, it should be taken as read that you think it's interesting. The whole point is to explain why - to tell people what's special about it. Does it present new evidence? If so, is it reliable? Does it introduce a new distinction, a new vocabulary, a new way of thinking? If so, why is it a good one?
Sadly it's easier to just call something interesting than to explain why it is. Partly this is because "interesting" (or "fascinating", "thought-provoking", "intriguing", "notable" etc.) is just one word, and it's easier to write one word than a sentence. More important is the fact that you probably don't know why you're interested by something until you do some thinking about it.
Don't duck out of doing that thinking. It's intellectual laziness. Even more so is to say that you're not sure if something is true, but it sure is interesting. "It's not necessarily true, but it's a fascinating thought" - is it? why?
Are you interested by the possibility that it's true, so if you learned that it was definitely false, it would become boring? Or is it one of those ideas that's interesting "in itself"? If so, why? Because it's an influential idea in a political or historical sense? Because it sheds light on the minds of the people who believe it? Are you sure that your interest isn't a kind of repressed belief? Are you really "only interested", or do you see something you like? If so, why not say so?
So, I'm quitting the habit, cold turkey, as of now. No more will I reach for the "interesting" button whenever I'm stuck for words. With any luck, this will make my writing a little bit more interes... hmm.
The War on "Interesting"
My New Year's Blog Resolution - no more calling things "interesting".
While writing, I sometimes find myself searching for an adjective to attach to something I've just mentioned, words to explain why I think it's relevant. It's... no... it's kind of... hmm... It's interesting, is what it is! Phew. Now I can move on. Anything can be "interesting" - a book, a blog post, an article, an event, an idea, a movement, a prediction, an argument.
Calling something interesting is effortless; easy; it's a one-size-fits-all term. If you can't think of anything else to say, you can at least say that. Which is why people do. I know I'm not alone in this.
But "interesting" is a cop-out. It adds nothing. If you're taking the trouble of writing about something, it should be taken as read that you think it's interesting. The whole point is to explain why - to tell people what's special about it. Does it present new evidence? If so, is it reliable? Does it introduce a new distinction, a new vocabulary, a new way of thinking? If so, why is it a good one?
Sadly it's easier to just call something interesting than to explain why it is. Partly this is because "interesting" (or "fascinating", "thought-provoking", "intriguing", "notable" etc.) is just one word, and it's easier to write one word than a sentence. More important is the fact that you probably don't know why you're interested by something until you do some thinking about it.
Don't duck out of doing that thinking. It's intellectual laziness. Even more so is to say that you're not sure if something is true, but it sure is interesting. "It's not necessarily true, but it's a fascinating thought" - is it? why?
Are you interested by the possibility that it's true, so if you learned that it was definitely false, it would become boring? Or is it one of those ideas that's interesting "in itself"? If so, why? Because it's an influential idea in a political or historical sense? Because it sheds light on the minds of the people who believe it? Are you sure that your interest isn't a kind of repressed belief? Are you really "only interested", or do you see something you like? If so, why not say so?
So, I'm quitting the habit, cold turkey, as of now. No more will I reach for the "interesting" button whenever I'm stuck for words. With any luck, this will make my writing a little bit more interes... hmm.
While writing, I sometimes find myself searching for an adjective to attach to something I've just mentioned, words to explain why I think it's relevant. It's... no... it's kind of... hmm... It's interesting, is what it is! Phew. Now I can move on. Anything can be "interesting" - a book, a blog post, an article, an event, an idea, a movement, a prediction, an argument.Calling something interesting is effortless; easy; it's a one-size-fits-all term. If you can't think of anything else to say, you can at least say that. Which is why people do. I know I'm not alone in this.
But "interesting" is a cop-out. It adds nothing. If you're taking the trouble of writing about something, it should be taken as read that you think it's interesting. The whole point is to explain why - to tell people what's special about it. Does it present new evidence? If so, is it reliable? Does it introduce a new distinction, a new vocabulary, a new way of thinking? If so, why is it a good one?
Sadly it's easier to just call something interesting than to explain why it is. Partly this is because "interesting" (or "fascinating", "thought-provoking", "intriguing", "notable" etc.) is just one word, and it's easier to write one word than a sentence. More important is the fact that you probably don't know why you're interested by something until you do some thinking about it.
Don't duck out of doing that thinking. It's intellectual laziness. Even more so is to say that you're not sure if something is true, but it sure is interesting. "It's not necessarily true, but it's a fascinating thought" - is it? why?
Are you interested by the possibility that it's true, so if you learned that it was definitely false, it would become boring? Or is it one of those ideas that's interesting "in itself"? If so, why? Because it's an influential idea in a political or historical sense? Because it sheds light on the minds of the people who believe it? Are you sure that your interest isn't a kind of repressed belief? Are you really "only interested", or do you see something you like? If so, why not say so?
So, I'm quitting the habit, cold turkey, as of now. No more will I reach for the "interesting" button whenever I'm stuck for words. With any luck, this will make my writing a little bit more interes... hmm.
Thursday, December 24, 2009
Feliz Navidad
It's Christmas Eve! I want to wish everyone a Merry Christmas. This is such a special time of year. Tonight I'm singing Ave Maria in the Children's Mass. I'm really excited! Last year, I got to be Mary.
Our Christmas tree is up. And all of our presents are wrapped. My Dad has been making lots of yummy food. I can't wait to eat our Christmas Eve dinner tonight!
Merry Chirstmas! I hope you get everything on your list! :) C
Wednesday, December 23, 2009
Good News for Armchair Neuropathologists
Ever wanted to crack the mysteries of the brain? Dreamed of discovering the cause of mental illness?Well, now, you can - or, at any rate, you can try - and you can do it from the comfort of your own home, thanks to the new Stanley Neuropathology Consortium Integrative Database.
Just register (it's free and instant) and you get access to a pool of data derived from the Stanley Neuropathology Consortium brain collection. The collection comprises 60 frozen brains - 15 each from people with schizophrenia, bipolar disorder, and clinical depression, and 15 "normals".
In a Neuropsychopharmacology paper announcing the project, administrators Sanghyeon Kim and Maree Webster point out that
Data sharing has become more important than ever in the biomedical sciences with the advance of high-throughput technology and web-based databases are one of the most efficient available resources to share datasets.The Institute's 60 brains have long been the leading source of human brain tissue for researchers in biological psychiatry. Whenever you read about a new discovery relating to schizophrenia or bipolar disorder, chances are the Stanley brains were involved. The Institute provide slices of the brains free of charge to scientists who request them, and they've sent out over 200,000 to date.
Until now, if you wanted to find out what these scientists discovered about the brains, you'd have to look up the results in the many hundreds of scientific papers where the various results were published. If you knew where to look, and if you had a lot of time on your hands. The database collates all of the findings. That's a good idea. To ensure that they get all of the results, the Institute have another good idea:
Coded specimens are sent to researchers with the code varying from researcher to researcher to ensure that all studies are blinded. The code is released to the researcher only when the data have been collected and submitted to the Institute.
The data we're provided about the brains is quite exciting, if you like molecules, comprising 1749 markers from 12 different parts of the brain. Markers include levels of proteins, RNA, and the number and shape of various types of cells.It's easy to use. While waiting for my coffee to brew, I compared the amount of the protein GFAP76 in the frontal cortex between the four groups. There was no significant difference. I guess GFAP76 doesn't cause mental illness - darn. So much for my Nobel Prize winning theory. But I did find that levels of GFAP76 were very strongly correlated with levels of another protein, "phosphirylated" (I think they mean "phosphorylated") PRKCA. You read it here first.
In the paper, Kim and Webster used the Database to find many differences between normal brains and diseased brains, including increased levels of dopamine in schizophrenia, and increased levels of glutamate in depression and bipolar. And decreased GAD67 proteins in the frontal cortex in bipolar and schizophrenia. And decreased reelin mRNA in the frontal cortex and cerebellum in bipolar and schizophrenia. And...
This leaves open the vital questions of what these differences mean, as I have complained before. And the problem with giving everyone in the world the results of 1749 different tests, and letting us cross-correlate them with each other and look for differences between 4 patient groups, is that you're making possible an awful lot of comparisons. With only 15 brains per group, none of the results can be considered anything more than provisional, anyway - what we really need are lots more brains.
But this database is still a welcome move. This kind of data pooling is the only sensible approach to doing modern science, and it's something people are advocating in other fields of neuroscience as well. It just makes sense to share results rather than leaving everyone to do there own thing in near-isolation from each other, now that we have the technology to do so. In fact, I'd say it's a... no-brainer.
Kim, S., & Webster, M. (2009). The Stanley Neuropathology Consortium Integrative Database: a Novel, Web-Based Tool for Exploring Neuropathological Markers in Psychiatric Disorders and the Biological Processes Associated with Abnormalities of Those Markers Neuropsychopharmacology, 35 (2), 473-482 DOI: 10.1038/npp.2009.151
Good News for Armchair Neuropathologists
Ever wanted to crack the mysteries of the brain? Dreamed of discovering the cause of mental illness?Well, now, you can - or, at any rate, you can try - and you can do it from the comfort of your own home, thanks to the new Stanley Neuropathology Consortium Integrative Database.
Just register (it's free and instant) and you get access to a pool of data derived from the Stanley Neuropathology Consortium brain collection. The collection comprises 60 frozen brains - 15 each from people with schizophrenia, bipolar disorder, and clinical depression, and 15 "normals".
In a Neuropsychopharmacology paper announcing the project, administrators Sanghyeon Kim and Maree Webster point out that
Data sharing has become more important than ever in the biomedical sciences with the advance of high-throughput technology and web-based databases are one of the most efficient available resources to share datasets.The Institute's 60 brains have long been the leading source of human brain tissue for researchers in biological psychiatry. Whenever you read about a new discovery relating to schizophrenia or bipolar disorder, chances are the Stanley brains were involved. The Institute provide slices of the brains free of charge to scientists who request them, and they've sent out over 200,000 to date.
Until now, if you wanted to find out what these scientists discovered about the brains, you'd have to look up the results in the many hundreds of scientific papers where the various results were published. If you knew where to look, and if you had a lot of time on your hands. The database collates all of the findings. That's a good idea. To ensure that they get all of the results, the Institute have another good idea:
Coded specimens are sent to researchers with the code varying from researcher to researcher to ensure that all studies are blinded. The code is released to the researcher only when the data have been collected and submitted to the Institute.
The data we're provided about the brains is quite exciting, if you like molecules, comprising 1749 markers from 12 different parts of the brain. Markers include levels of proteins, RNA, and the number and shape of various types of cells.It's easy to use. While waiting for my coffee to brew, I compared the amount of the protein GFAP76 in the frontal cortex between the four groups. There was no significant difference. I guess GFAP76 doesn't cause mental illness - darn. So much for my Nobel Prize winning theory. But I did find that levels of GFAP76 were very strongly correlated with levels of another protein, "phosphirylated" (I think they mean "phosphorylated") PRKCA. You read it here first.
In the paper, Kim and Webster used the Database to find many differences between normal brains and diseased brains, including increased levels of dopamine in schizophrenia, and increased levels of glutamate in depression and bipolar. And decreased GAD67 proteins in the frontal cortex in bipolar and schizophrenia. And decreased reelin mRNA in the frontal cortex and cerebellum in bipolar and schizophrenia. And...
This leaves open the vital questions of what these differences mean, as I have complained before. And the problem with giving everyone in the world the results of 1749 different tests, and letting us cross-correlate them with each other and look for differences between 4 patient groups, is that you're making possible an awful lot of comparisons. With only 15 brains per group, none of the results can be considered anything more than provisional, anyway - what we really need are lots more brains.
But this database is still a welcome move. This kind of data pooling is the only sensible approach to doing modern science, and it's something people are advocating in other fields of neuroscience as well. It just makes sense to share results rather than leaving everyone to do there own thing in near-isolation from each other, now that we have the technology to do so. In fact, I'd say it's a... no-brainer.
Kim, S., & Webster, M. (2009). The Stanley Neuropathology Consortium Integrative Database: a Novel, Web-Based Tool for Exploring Neuropathological Markers in Psychiatric Disorders and the Biological Processes Associated with Abnormalities of Those Markers Neuropsychopharmacology, 35 (2), 473-482 DOI: 10.1038/npp.2009.151
Monday, December 21, 2009
Yummy Comida!
Dad made some yummy green chili stew and tortillas tonight for dinner. It was so good. And it warmed us all up. It's so cold outside! I ate 2 bowls of stew and 3 tortillas. 1 of them with butter. Fresh off the placa. It was the best one!
I also made a chocolate cake. Mi abuelita helped me with the frosting. We make our own. It is so yummy! I baked 2 cakes and we stacked them. Mi abuelita make some chocolate and raspberry filling to put between them. And then we frosted the cake with chocolate icing. After dinner, we each had a big piece with a glass of milk. My belly is all full now!
Tonight, I need to work on dad's Christmas present. I only have a few days left to finish it! But it's almost done. I'm not too worried about it yet. I think I can finish it tonight. Maybe in the morning. I'm not sure. But that is what I'm working on tonight. :) C
I also made a chocolate cake. Mi abuelita helped me with the frosting. We make our own. It is so yummy! I baked 2 cakes and we stacked them. Mi abuelita make some chocolate and raspberry filling to put between them. And then we frosted the cake with chocolate icing. After dinner, we each had a big piece with a glass of milk. My belly is all full now!
Tonight, I need to work on dad's Christmas present. I only have a few days left to finish it! But it's almost done. I'm not too worried about it yet. I think I can finish it tonight. Maybe in the morning. I'm not sure. But that is what I'm working on tonight. :) C
The Guineapigs
Before waterboarding, there was wall standing.The Guineapigs is a book by John McGuffin. It was published in 1974, at the height of "The Troubles" in Northern Ireland, and banned in Britain almost immediately.
The "guineapigs" in question were 14 men from Northern Ireland detained by British security forces during the 1971 campaign of internment of suspected Irish Republican Army militants and sympathizers. The book details the treatment they experienced in the week after their detention, specifically "sensory deprivation".
The men were forced to stand up against a wall, with a black hood over their head, in a room into which a loud noise - described as something like a jet engine or gushing water - was played. If they fell or otherwise moved from this stance, they were forced back up. This went on for up to 48 hours, during which time they were given neither food nor sleep.
After this the treatment became a bit less harsh, and they were interrogated at various intervals. After about a week, they were released into a "normal" prison, and the story came out. A government inquiry, the Compton Report, followed, confirming that the "Questioning in Depth" had occurred but denying that it constituted "brutality".
The Guineapigs contains first person accounts from several of the men, describing the disorientation, hallucinations and terror they experienced during the procedure, and also details the psychological after-effects they reportedly suffered, including several cases of mental illness and at least psychiatric hospitalization.
McGuffin's most controversial claim was that the whole thing was a psychological experiment. It could not, he said, have been meant to gather useful information per se, because the 14 "subjects" were not especially high-value suspects; they seemed to have been chosen at random from the hundreds interned. Instead, he said, it was a research project, a trial of the technique of sensory deprivation as torture.
During the 1960s and 1970s there was lots of academic research on sensory deprivation, in which volunteers often reported hallucinations, paranoia, mood changes and other "psychotic" symptoms after being deprived of sight, sound and touch stimuli for a few hours. According to McGuffin, the British government decided to "field test" to procedure to see whether the same thing happened in "real life" with test subjects who weren't willing volunteers.
I'm not sure whether to believe this explanation of what happened; McGuffin was hardly an unbiased observer - he was himself interned in 1971, although he wasn't amongst the guineapigs - and he was a lifelong opponent of British rule in Northern Ireland. We'll probably never know for sure. But maybe it's as convincing as any other explanation.
Links: Lots of the book is online here. Mind Hacks on a recent sensory deprivation study, and a documentary about s.d. interrogation during WW2. I found a paper by T Shallice (1972) on The Ulster depth interrogation techniques and their relation to sensory deprivation research, but I haven't been able to access it yet. John McGuffin obits.
The Guineapigs
Before waterboarding, there was wall standing.The Guineapigs is a book by John McGuffin. It was published in 1974, at the height of "The Troubles" in Northern Ireland, and banned in Britain almost immediately.
The "guineapigs" in question were 14 men from Northern Ireland detained by British security forces during the 1971 campaign of internment of suspected Irish Republican Army militants and sympathizers. The book details the treatment they experienced in the week after their detention, specifically "sensory deprivation".
The men were forced to stand up against a wall, with a black hood over their head, in a room into which a loud noise - described as something like a jet engine or gushing water - was played. If they fell or otherwise moved from this stance, they were forced back up. This went on for up to 48 hours, during which time they were given neither food nor sleep.
After this the treatment became a bit less harsh, and they were interrogated at various intervals. After about a week, they were released into a "normal" prison, and the story came out. A government inquiry, the Compton Report, followed, confirming that the "Questioning in Depth" had occurred but denying that it constituted "brutality".
The Guineapigs contains first person accounts from several of the men, describing the disorientation, hallucinations and terror they experienced during the procedure, and also details the psychological after-effects they reportedly suffered, including several cases of mental illness and at least psychiatric hospitalization.
McGuffin's most controversial claim was that the whole thing was a psychological experiment. It could not, he said, have been meant to gather useful information per se, because the 14 "subjects" were not especially high-value suspects; they seemed to have been chosen at random from the hundreds interned. Instead, he said, it was a research project, a trial of the technique of sensory deprivation as torture.
During the 1960s and 1970s there was lots of academic research on sensory deprivation, in which volunteers often reported hallucinations, paranoia, mood changes and other "psychotic" symptoms after being deprived of sight, sound and touch stimuli for a few hours. According to McGuffin, the British government decided to "field test" to procedure to see whether the same thing happened in "real life" with test subjects who weren't willing volunteers.
I'm not sure whether to believe this explanation of what happened; McGuffin was hardly an unbiased observer - he was himself interned in 1971, although he wasn't amongst the guineapigs - and he was a lifelong opponent of British rule in Northern Ireland. We'll probably never know for sure. But maybe it's as convincing as any other explanation.
Links: Lots of the book is online here. Mind Hacks on a recent sensory deprivation study, and a documentary about s.d. interrogation during WW2. I found a paper by T Shallice (1972) on The Ulster depth interrogation techniques and their relation to sensory deprivation research, but I haven't been able to access it yet. John McGuffin obits.
Sunday, December 20, 2009
Neuroskeptic Gets "Cited"
...kind of. Last week, I blogged about a Nature paper, Eisenegger et al, reporting that giving women testosterone makes them behave more generously in a money-sharing procedure called the Ultimatum Game.
But just a few days later, PLoS ONE published a paper, Zak et al, finding exactly the opposite result - testosterone decreased generosity in the Ultimatum Game - although that was in men, rather than women. The lead author of the PLoS paper, Paul J. Zak, then "cited" my blog post in an online comment attached to his article, as part of a discussion of the differences between his paper and Eisenegger et al's. This is not a proper citation of course, but it's a start. At least I like to think so.
PLoS have a brilliant policy of having a blog-style comment thread attached to every paper. This is a far better system than the traditional academic policy of allowing comments only in the form of formal "Letters to the Editor" of the journal. This made sense in the days before the internet, but it's long outlived its usefulness.
A Letter has to be approved by the editor of the journal to get published at all. For reasons of space, if nothing else, the number which get printed is small. Even if your Letter does see the light of day, it will be, at minimum, a couple of months after the original paper was published, by which time most readers of the original will have forgotten what the fuss was about. If the original authors reply to your Letter, and you want to reply to their reply, it'll be another couple of months before you can, assuming you still care about it by this point. And so on.
An online comment thread, on the other hand, is "peer review" in its purest form. The key difference is speed - replies take place in real time or close to it, which makes a genuine conversation possible. The fact that anyone on the internet can comment might not seem to be a good thing; the internet makes you stupid, after all. But the standard of comments on PLoS papers is generally very high; I don't know if this is because of a moderation policy, or just because PLoS readers are sensible folk.
A few other journals have adopted a similar commenting system, notably Nature (although apparently not other Nature group journals like Nature Neuroscience), but this is something I'd like to see all journals adopt. Ultimately, I'd like to see the boundaries between the "official" academic literature and "informal" online discussion such as blogs blurred further; PLoS seem to be leading the way in this regard too with their recently announced integration with ResearchBlogging.org although Nature also have a blog section. Exciting times.
But just a few days later, PLoS ONE published a paper, Zak et al, finding exactly the opposite result - testosterone decreased generosity in the Ultimatum Game - although that was in men, rather than women. The lead author of the PLoS paper, Paul J. Zak, then "cited" my blog post in an online comment attached to his article, as part of a discussion of the differences between his paper and Eisenegger et al's. This is not a proper citation of course, but it's a start. At least I like to think so.
PLoS have a brilliant policy of having a blog-style comment thread attached to every paper. This is a far better system than the traditional academic policy of allowing comments only in the form of formal "Letters to the Editor" of the journal. This made sense in the days before the internet, but it's long outlived its usefulness.A Letter has to be approved by the editor of the journal to get published at all. For reasons of space, if nothing else, the number which get printed is small. Even if your Letter does see the light of day, it will be, at minimum, a couple of months after the original paper was published, by which time most readers of the original will have forgotten what the fuss was about. If the original authors reply to your Letter, and you want to reply to their reply, it'll be another couple of months before you can, assuming you still care about it by this point. And so on.
An online comment thread, on the other hand, is "peer review" in its purest form. The key difference is speed - replies take place in real time or close to it, which makes a genuine conversation possible. The fact that anyone on the internet can comment might not seem to be a good thing; the internet makes you stupid, after all. But the standard of comments on PLoS papers is generally very high; I don't know if this is because of a moderation policy, or just because PLoS readers are sensible folk.
A few other journals have adopted a similar commenting system, notably Nature (although apparently not other Nature group journals like Nature Neuroscience), but this is something I'd like to see all journals adopt. Ultimately, I'd like to see the boundaries between the "official" academic literature and "informal" online discussion such as blogs blurred further; PLoS seem to be leading the way in this regard too with their recently announced integration with ResearchBlogging.org although Nature also have a blog section. Exciting times.
Neuroskeptic Gets "Cited"
...kind of. Last week, I blogged about a Nature paper, Eisenegger et al, reporting that giving women testosterone makes them behave more generously in a money-sharing procedure called the Ultimatum Game.
But just a few days later, PLoS ONE published a paper, Zak et al, finding exactly the opposite result - testosterone decreased generosity in the Ultimatum Game - although that was in men, rather than women. The lead author of the PLoS paper, Paul J. Zak, then "cited" my blog post in an online comment attached to his article, as part of a discussion of the differences between his paper and Eisenegger et al's. This is not a proper citation of course, but it's a start. At least I like to think so.
PLoS have a brilliant policy of having a blog-style comment thread attached to every paper. This is a far better system than the traditional academic policy of allowing comments only in the form of formal "Letters to the Editor" of the journal. This made sense in the days before the internet, but it's long outlived its usefulness.
A Letter has to be approved by the editor of the journal to get published at all. For reasons of space, if nothing else, the number which get printed is small. Even if your Letter does see the light of day, it will be, at minimum, a couple of months after the original paper was published, by which time most readers of the original will have forgotten what the fuss was about. If the original authors reply to your Letter, and you want to reply to their reply, it'll be another couple of months before you can, assuming you still care about it by this point. And so on.
An online comment thread, on the other hand, is "peer review" in its purest form. The key difference is speed - replies take place in real time or close to it, which makes a genuine conversation possible. The fact that anyone on the internet can comment might not seem to be a good thing; the internet makes you stupid, after all. But the standard of comments on PLoS papers is generally very high; I don't know if this is because of a moderation policy, or just because PLoS readers are sensible folk.
A few other journals have adopted a similar commenting system, notably Nature (although apparently not other Nature group journals like Nature Neuroscience), but this is something I'd like to see all journals adopt. Ultimately, I'd like to see the boundaries between the "official" academic literature and "informal" online discussion such as blogs blurred further; PLoS seem to be leading the way in this regard too with their recently announced integration with ResearchBlogging.org although Nature also have a blog section. Exciting times.
But just a few days later, PLoS ONE published a paper, Zak et al, finding exactly the opposite result - testosterone decreased generosity in the Ultimatum Game - although that was in men, rather than women. The lead author of the PLoS paper, Paul J. Zak, then "cited" my blog post in an online comment attached to his article, as part of a discussion of the differences between his paper and Eisenegger et al's. This is not a proper citation of course, but it's a start. At least I like to think so.
PLoS have a brilliant policy of having a blog-style comment thread attached to every paper. This is a far better system than the traditional academic policy of allowing comments only in the form of formal "Letters to the Editor" of the journal. This made sense in the days before the internet, but it's long outlived its usefulness.A Letter has to be approved by the editor of the journal to get published at all. For reasons of space, if nothing else, the number which get printed is small. Even if your Letter does see the light of day, it will be, at minimum, a couple of months after the original paper was published, by which time most readers of the original will have forgotten what the fuss was about. If the original authors reply to your Letter, and you want to reply to their reply, it'll be another couple of months before you can, assuming you still care about it by this point. And so on.
An online comment thread, on the other hand, is "peer review" in its purest form. The key difference is speed - replies take place in real time or close to it, which makes a genuine conversation possible. The fact that anyone on the internet can comment might not seem to be a good thing; the internet makes you stupid, after all. But the standard of comments on PLoS papers is generally very high; I don't know if this is because of a moderation policy, or just because PLoS readers are sensible folk.
A few other journals have adopted a similar commenting system, notably Nature (although apparently not other Nature group journals like Nature Neuroscience), but this is something I'd like to see all journals adopt. Ultimately, I'd like to see the boundaries between the "official" academic literature and "informal" online discussion such as blogs blurred further; PLoS seem to be leading the way in this regard too with their recently announced integration with ResearchBlogging.org although Nature also have a blog section. Exciting times.
Friday, December 18, 2009
FELIZ NATAL A TODOS!!
CURIOSA SAI DE FÉRIAS MAS LEVA VOCÊ NO CORAÇÃO.
SENTIREI MUITAS SAUDADES SUAS.
VOLTAREI EM JANEIRO. PASSAREI O NATAL COM A MINHA FAMILIA. AGRADEÇO A SUA AMIZADE, O SEU CARINHO E O SEU AMOR.
COM VOCÊ FUI MUITO FELIZ.
APRENDI MUITO COM VOCÊ NESTE, ANO.
MUITO OBRIGADO PELA SUA COMPANHIA.
ESTOU INDO, MAS LEVAREI VOCÊ JUNTO NO MEU CORAÇÃO.
DEIXO ESTE CARTÃO DE FELIZ NATAL E PRÓSPERO ANO NOVO!
DEIXO ESSES CANTINHOS PARA VOCÊ VISITAR NA MINHA AUSÊNCIA.
VENHA REGISTRE. NA VOLTA EU SEGUIREI AS MARCAS E CHEGAREI ATÉ VOCÊ!
Poetas-Um Vôo Livre
Sinal de Liberdade-uma expressão de sentimento
Blog Coletivo-Uma Interação de Amigos
Meus Mimos!
VENHA REGISTRE. NA VOLTA EU SEGUIREI AS MARCAS E CHEGAREI ATÉ VOCÊ!
Poetas-Um Vôo Livre
Sinal de Liberdade-uma expressão de sentimento
Blog Coletivo-Uma Interação de Amigos
Meus Mimos!
Two Drugs Are Better Than One?
According to a study just out in the American Journal of Psychiatry, starting depressed people on two antidepressants leads to much better results than starting them on just one - Combination of Antidepressant Medications From Treatment Initiation for Major Depressive Disorder. But how reliable is it?Currently accepted practice is to prescribe one antidepressant to begin with, and if the patient doesn't feel better after about 6 weeks, to either change to a different antidepressant (switching) or add a second drug while continuing the first (augmentation).
But in clinical trials and also in "real life", the proportion of depressed people who achieve "remission", meaning that they're fully or almost fully recovered, with their first antidepressant is rarely more than 1 in 3. Some antidepressants may be slightly better than others as first-line treatments, but any such differences are small.
Do two mediocre drugs combined add up to one good treatment? In this study, Blier et al. took 105 depressed people and gave them either one antidepressant or two. The one antidepressant was fluoxetine (Prozac) 20mg, and the two was mirtazapine 30mg and either fluoxetine 20mg, venlafaxine 225mg, or buproprion 150mg. The study was double-blind; patients didn't know which drug(s) they were on. There was no placebo group, however.
Mirtazapine (Remeron) is an antidepressant which is commonly used as an add-on treatment in depression, because it can be safely combined with most other drugs. So it makes sense to use mirtazapine in research like this, but take note: this study was "supported by Organon Pharmaceuticals", who make... mirtazapine.
What happened? All three combinations of two antidepressants were equally effective, and all three were considerably better than just Prozac alone, in the initial 6 week phase of the trial. The difference was massive by the standards of antidepressants - about 5 Hamilton scale points, considerably larger than the average benefit of an antidepressant over placebo.There was also a 6 month follow-up phase to the study in which everyone who had been taking two antidepressants had one of them replaced by placebos, so everyone ended up only taking one drug (either fluoxetine or mirtazapine). Discontinuing one antidepressant seemed to cause relapse in about 40-50% of the people who were taking two, as opposed to a 25% relapse rate in the people who started on just fluoxetine and kept taking it. If you believe it, this is further evidence that two drugs are better than one, although the total sample size was just 66 for this bit, and I'm not sure I do.
What are we to make of all this? This study joins a previous one finding that mirtazapine plus paroxetine is better than either drug alone as a starting treatment. But that paper was also by Blier et al and it was "fully funded by Organon Pharmaceuticals" although apparently "The sponsor had no role in the study design, in the collection and interpretation of the data, in the preparation of this report, and in the decision to publish this manuscript".
Personally, I'm not so much troubled by the industry sponsorship in these studies as I am by the nature of the add-on treatment, mirtazapine. Mirtazapine is an unusual drug, with a pharmacological profile very different to that of most antidepressants. Notably, it's a powerful hypnotic - it makes you sleep - and it increases appetite. Patients on mirtazapine in the present study put on over 2kg in 6 weeks.
Why does this matter? Because the two scales used to rate depression in this study, the Hamilton Scale and the Montgomery-Asberg Scale, both count reduced appetite and sleeplessness as symptoms of depression. If you're on mirtazapine, you're unlikely to have either problem - you'll be more worried about the exact opposite, insatiable hunger and drowsiness. So mirtazapine could reduce your total score on these scales even if it didn't change your mood. I have no idea to what extent this is a factor in these results, but it could be important.
So, are two drugs better than one? Should antidepressants come with a side-order of mirtazapine as standard? Maybe. But it's far from proven.
Blier, P., Ward, H., Tremblay, P., Laberge, L., Hebert, C., & Bergeron, R. (2009). Combination of Antidepressant Medications From Treatment Initiation for Major Depressive Disorder: A Double-Blind Randomized Study American Journal of Psychiatry DOI: 10.1176/appi.ajp.2009.09020186
Two Drugs Are Better Than One?
According to a study just out in the American Journal of Psychiatry, starting depressed people on two antidepressants leads to much better results than starting them on just one - Combination of Antidepressant Medications From Treatment Initiation for Major Depressive Disorder. But how reliable is it?Currently accepted practice is to prescribe one antidepressant to begin with, and if the patient doesn't feel better after about 6 weeks, to either change to a different antidepressant (switching) or add a second drug while continuing the first (augmentation).
But in clinical trials and also in "real life", the proportion of depressed people who achieve "remission", meaning that they're fully or almost fully recovered, with their first antidepressant is rarely more than 1 in 3. Some antidepressants may be slightly better than others as first-line treatments, but any such differences are small.
Do two mediocre drugs combined add up to one good treatment? In this study, Blier et al. took 105 depressed people and gave them either one antidepressant or two. The one antidepressant was fluoxetine (Prozac) 20mg, and the two was mirtazapine 30mg and either fluoxetine 20mg, venlafaxine 225mg, or buproprion 150mg. The study was double-blind; patients didn't know which drug(s) they were on. There was no placebo group, however.
Mirtazapine (Remeron) is an antidepressant which is commonly used as an add-on treatment in depression, because it can be safely combined with most other drugs. So it makes sense to use mirtazapine in research like this, but take note: this study was "supported by Organon Pharmaceuticals", who make... mirtazapine.
What happened? All three combinations of two antidepressants were equally effective, and all three were considerably better than just Prozac alone, in the initial 6 week phase of the trial. The difference was massive by the standards of antidepressants - about 5 Hamilton scale points, considerably larger than the average benefit of an antidepressant over placebo.There was also a 6 month follow-up phase to the study in which everyone who had been taking two antidepressants had one of them replaced by placebos, so everyone ended up only taking one drug (either fluoxetine or mirtazapine). Discontinuing one antidepressant seemed to cause relapse in about 40-50% of the people who were taking two, as opposed to a 25% relapse rate in the people who started on just fluoxetine and kept taking it. If you believe it, this is further evidence that two drugs are better than one, although the total sample size was just 66 for this bit, and I'm not sure I do.
What are we to make of all this? This study joins a previous one finding that mirtazapine plus paroxetine is better than either drug alone as a starting treatment. But that paper was also by Blier et al and it was "fully funded by Organon Pharmaceuticals" although apparently "The sponsor had no role in the study design, in the collection and interpretation of the data, in the preparation of this report, and in the decision to publish this manuscript".
Personally, I'm not so much troubled by the industry sponsorship in these studies as I am by the nature of the add-on treatment, mirtazapine. Mirtazapine is an unusual drug, with a pharmacological profile very different to that of most antidepressants. Notably, it's a powerful hypnotic - it makes you sleep - and it increases appetite. Patients on mirtazapine in the present study put on over 2kg in 6 weeks.
Why does this matter? Because the two scales used to rate depression in this study, the Hamilton Scale and the Montgomery-Asberg Scale, both count reduced appetite and sleeplessness as symptoms of depression. If you're on mirtazapine, you're unlikely to have either problem - you'll be more worried about the exact opposite, insatiable hunger and drowsiness. So mirtazapine could reduce your total score on these scales even if it didn't change your mood. I have no idea to what extent this is a factor in these results, but it could be important.
So, are two drugs better than one? Should antidepressants come with a side-order of mirtazapine as standard? Maybe. But it's far from proven.
Blier, P., Ward, H., Tremblay, P., Laberge, L., Hebert, C., & Bergeron, R. (2009). Combination of Antidepressant Medications From Treatment Initiation for Major Depressive Disorder: A Double-Blind Randomized Study American Journal of Psychiatry DOI: 10.1176/appi.ajp.2009.09020186
CAMPANHIA SOLIDARIEDADE.
"A CAMINHO DO MEU SONHO"
ou aqui http://clubedasmulheresbeiras.blogspot.com/2009/12/juntos-vamos-ajudar-isabela-no-caminho_09.html
ESTA LINDA MOÇA, CHAMADA ISABELA, PRECISA DE SUA AJUDA.
CADA COMENTÁRIO LÁ COLETIVA DE NATAL DE MINHA ALDEIA VALE UMA LUZ...
CURIOSA RESOLVEU AJUDAR NA DIVULGAÇÃO. FAÇA A SUA PARTE.
LEIA O TEXTO E PASSE PARA COMENTAR NO ENDEREÇO ABAIXO.
(infelizmente a foto não apareceu).
clik no link acima, e terá mais informação.
EIS O TEXTO RECEBIDO:
CLIQUE AQUI E DEIXE TAMBÉM O SEU COMENTÁRIO LÁ.
http://aldeiadaminhavida.blogspot.com/2009/12/natal-na-minha-terra-gramadocanela.html#comments
MUITO OBRIGADA PELO SEU CARINHO.
VAJUDANDO A ISABELA, ESTAREMOS FAZENDO PARTE DO PROJETO GENEROSIDADE.
VALEU MEUS QUERIDOS.
SANDRA
ESTE SELO É SEU AMIGO(A)
VENHA LER OS TEXTOS.
VENHA INTERAGIR COM
ESTE BLOG.
VENHA INTERAGIR COM
ESTE BLOG.
Thursday, December 17, 2009
Christmas Presents
Last year I got to make a lot of Christmas presents. My Nana helped me every week. We started when school started. I finished my presents right before Christmas. I had lots of fun!
This year I think my Nana had more classes. I know she is working more. She is studying to be a doctor. We didn't get to spend a lot of time together. She wasn't able to pick me up from school every Wednesday. Only 1 week in the month. But it is ok. I know she is trying to make kids feel better.
I have been trying to work on my projects by myself. I have a bunch of things made. 1 for my Nana, 1 for my Nono, my abuelitas, my Dad, and the girls. I have 8 little friends. I think I might get done on time. I wrapped a few of them. When I get stuck I put my project away. I wait until I can see my Nana to ask for help.
I gave my friends at school their stockings I made. Nana helped me to make those. My dad took me shopping for stuff to put inside. My friends were really happy. 1 of my friends never had a stocking before. She told me that she was going to hang hers up at her house. I'm glad she liked it! :) C
O LAÇO E O ABRAÇO.
QUERO DEIXAR O MEU ABRAÇO A TODOS.
ESTA SENDO MARAVILHOSO TER A SUA COMPANHIA.
ME SINTO MUITO FELIZ, PELA LINDA CONQUISTA DESTE ANO. MUITOAS AMIGOS EU ENCONTREI AQUI.
NÃO IMAGINEI QUE FOSSE POSSIÍVEL. MAS É POSSÍVEL, SIM, QUANDO A AMIZADE É VERDADEIRA E RECIPROCA.
VAI O MEU ABRAÇO A TODOS E UM LAÇO DE CARINHO.
APROVEITO AINDA PARA ME DESCULPAR PELAS ATRASOS DAS VISITAS. ESTÁ MUITO CORRIDO. ESTOU PASSANDO PELOS MÉDICOS, ANTES DE FEXHAR O ANO. E É TUDO NESTA SEMANA. AMANHÃ IREI DE NOVO.
QUANTO AO MEU PÉ SOMENTE EM FEVEVEIRO PARA RETORNAR A PISAR. MAS ESTAREMOS DE MULETA, ESPERANDO O PAPAI NOEL CHEGAR E O ANO NOVO.
O IMPORTANTE É A VIDA.
OBRIGADA A TODOS.
FICA MEU LAÇO E O MEU ABRAÇO.
DEIXO A TODOS O MEU ABRAÇO E O MEU, MAIS SINCEROS AGRADECIMENTOS, POR ESTA AMIZADE, MARAVILHOSA DE TODAS AS MANHÃS. QUANDO RECEBI ESTA MENSAGEM, LEMBREI-ME LOGO DE VOCÊ MEU AMIGA(O), VIRTUAL. COM É BOM PODER TERMOS CONQUISTADOS LAÇOS DE TERNURAS E CARINHO. DEIXO MEU LAÇO E O MEU ABRAÇO. MUITO OBRIGADA PELA SUA COMPANHIA.
CURIOSA JÁ ATINGIU O NÚMERO DE 250 SEGUIDORES, ATÉ JÁ PASSOU. A CADA 50 SEGUIDORES A MAIS, A (O) FELIZERDO, GANHA O SELO ESPECIAL.
ENTÃO A MINHA SEGUIDORA DESSA VEZ, É A REGINA.
MAS NÃO CONSEGUI LOCALIZÁ-LA. DEIXEI RECADO NO BLOG DA SONIA REGINA.
SEI QUE LOGO ELA VIRA.
EM ESPECIAL A REGINA.
MAS TODOS PODERÃO LEVAR ESTA LINDA RODA.É DE TODOS.
COM MUITO CARINHO
SANDRA
AQUI TEM MAIS MAIS MIMOS.
Meus Mimos!
SE VOCÊ AINDA NÃO CONHECE, VENHA. EU TE ESPERO.
Poetas-Um Vôo Livre
Sinal de Liberdade-uma expressão de sentimento
Blog Coletivo-Uma Interação de Amigos
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