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Grow your brain, get happy
This is a post continuing a little exchange between me and megan regarding a relation between antidepressants and brain growth.
The antidepressants that are being referred to in "Proust was a neuroscientist" are fluoxetine, tianeptine, and desipramine. They're all in the market, except for tianeptine, which is only approved in France.
From the link:
http://en.wikipedia.org/wiki/Brain-derived_neurotrophic_factor
So this suggests to me that things are still a little inconclusive, but from what I can see, the relation that's being speculated upon here is this. Serotonin is an inhibitory neurochemical, and it tends to slow down dopamine activity. High dopamine activity is related to running thoughts and resultant stress [And therefore lowered levels of BDNF from the corticosterone] - Think about it, when you drink coffee or take other dopamine-increasing stimulants, how do your thoughts work? Mine tend to become a lot more focused, and sometimes I get thoughts that are kind of hard to focus away from. When it comes to feeling down about something, the same sort of thought patterns in relation to that something are very apparent. These kinds of running thoughts that just won't quit are at the heart of the cause of depression. We also have MDMA treatment - MDMA is also a serotonin reuptake inhibitor, and in therapy, it's used to make those thoughts related to stress (And one of the main disorders treated with MDMA therapy is post-traumatic stress disorder, to make my point clearer) on a subject more inconsequential for a short period of time so that the subject relating to those stressful thoughts can be talked about openly.
So, it seems to me that this isn't so much about brain growth causing happiness, but happiness causing brain growth!
megan Sat, Dec 29, 2007
Perhaps variety of anti-depressants he's talking about are just now in the works and not yet on the market, but this is a quote from the book:
Other scientists have discovered that antidepressants work by stimulating neurogenesis (at least in rodents), implying that depression is ultimately caused by a decrease in the amount of new neurons, and not by a lack of serotonin. A new class of anti-depressants is being developed that targets the neurogenesis pathway.
to resolve the misunderstanding, i'm more interested in how inducing the growth of new brain cells makes people happy than in prescription medications that may or may not get you there.
The antidepressants that are being referred to in "Proust was a neuroscientist" are fluoxetine, tianeptine, and desipramine. They're all in the market, except for tianeptine, which is only approved in France.
From the link:
One possible explanation for this action is the brain-derived growth factor (BDNF). BDNF is regulated by levels of serotonin and is known to be a prime candidate for causing serotonin axon growth, Koliatsos said.
In general, the relationships between brain serotonin concentrations and BDNF expression are very complex, but previous studies have suggested that both higher (such as caused by serotonin reuptake inhibitors) and lower (such as effected by tianeptine) concentrations of free serotonin might induce BDNF expression in such brain regions as the frontal and parietal cortex.
The researchers caution that since a previous study failed to show a correlation between tianeptine treatment and BDNF levels, further investigation of the complex regulations of BDNF by antidepressants is needed.
http://en.wikipedia.org/wiki/Brain-derived_neurotrophic_factor
Effects of stress and BDNF's link in depression
Exposure to stress and the stress hormone corticosterone has been shown to decrease the expression of BDNF in rats, and leads to an eventual atrophy of the hippocampus if exposure is persistent. Similar atrophy has been shown to take place in humans suffering from chronic depression. In addition, rats bred to be heterozygous for BDNF, therefore reducing its expression, have been observed to exhibit similar hippocampal atrophy, suggesting that an etiological link between the development of depressive illness and regulation of BDNF exists. On the other hand, the excitatory neurotransmitter glutamate, voluntary exercise, caloric restriction, intellectual stimulation, and various treatments for depression (such as antidepressants and electroconvulsive therapy) strongly increase expression of BDNF in the brain, and have been shown to protect against this atrophy.
So this suggests to me that things are still a little inconclusive, but from what I can see, the relation that's being speculated upon here is this. Serotonin is an inhibitory neurochemical, and it tends to slow down dopamine activity. High dopamine activity is related to running thoughts and resultant stress [And therefore lowered levels of BDNF from the corticosterone] - Think about it, when you drink coffee or take other dopamine-increasing stimulants, how do your thoughts work? Mine tend to become a lot more focused, and sometimes I get thoughts that are kind of hard to focus away from. When it comes to feeling down about something, the same sort of thought patterns in relation to that something are very apparent. These kinds of running thoughts that just won't quit are at the heart of the cause of depression. We also have MDMA treatment - MDMA is also a serotonin reuptake inhibitor, and in therapy, it's used to make those thoughts related to stress (And one of the main disorders treated with MDMA therapy is post-traumatic stress disorder, to make my point clearer) on a subject more inconsequential for a short period of time so that the subject relating to those stressful thoughts can be talked about openly. So, it seems to me that this isn't so much about brain growth causing happiness, but happiness causing brain growth!
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