depression
Magical thinking and feelings of control
Oct 3rd
A recent article in Science Magazine relates Magical thinking to feelings of control. It is an interesting paper and here is the abstract:
We present six experiments that tested whether lacking control increases illusory pattern perception,which we define as the identification of a coherent and meaningful interrelationship among a set of random or unrelated stimuli. Participants who lacked control were more likely to perceive a variety of illusory patterns, including seeing images in noise, forming illusory correlations in stock market information, perceiving conspiracies, and developing superstitions. Additionally, we demonstrated that increased pattern perception has a motivational basis by measuring the need for structure directly and showing that the causal link between lack of control and illusory pattern perception is reduced by affirming the self. Although these many disparate forms of pattern perception are typically discussed as separate phenomena, the current results suggest that there is a common motive underlying them.
Encephalon Emerald Edition
Sep 29th
The emerald Edition of Encephalon is just out at the Neuroscientifically challenged and Marc does a good job of bringing to light some of the most interesting and fascinating posts on brain from the last two weeks. A few that I found immediately drawn to were Greg Downey’s critical appraisal of the neuroplasticity popular press misconceptions and he does a pretty good job of that while simultaneously arousing interest in neuroplasticity in general and Doidge’s book in particular. another goo done is the growing recognition that antidepressant can temporarily increase suicide risk and that anti-psychotics may be a novel treatment for reducing suicide risk as they help control impulsivity. To me dopamine is related to impulsivity and anti-psychotics seem a better bet than anti-depressants when targeting suicide as most suicide is due to high impulsivity. There are many more gems, so go have a look.
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Suicide Prevention: steps to keep the impulse in check!
Jul 10th
New York Times has a very interesting and well-written piece on the ‘how’ or mechanisms of suicide consummation and how simple steps like reducing access to guns, or erecting barriers on bridges which are at a height, or even simple things like not packing tablets in bottles , but in pouches, so that it takes time to remove the pills form their containers before an overdose can be taken; can lead to big reduction in suicide rates as the few extra efforts or time needed to commit the act, is often enough to dissuade people from acting on their impulse.
It is a very nice post and is a must reading for everyone, especially mental-health workers and those involved in making public policies as it dispels the myth that those hell-bent on taking their lives will go to any length to do so and will find alternative mechanisms if one mechanism is made costly.
Thanks to Mind Hacks for bringing this to my attention!
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Antidepressants and neurogenesis / plasticity
Apr 23rd
It is relatively less well known that much of the anti-depressant effect of medications like Prozac may be due to them leading to better neurogenesis in the brain/ hippocampus. It is more well known that depression may itself be caused due to reduced neurogenesis. What is most well known is the scientifically unproved ‘serotonin’ theory of depression and how SSRIs work by increasing the level of serotonin in the brain.
Now a new research paper shows that Prozac has a non-specific effect on plasticity ion the brain and can even be used to treat Ambylopia, a defect of visual system, by rewiring the brain. Here is the abstract:
We investigated whether fluoxetine, a widely prescribed medication for treatment of depression, restores neuronal plasticity in the adult visual system of the rat. We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pathophysiology of mood disorders.
Now this brings me to an important conclusion. We have shown earlier that depression is associated with a bland sense of taste and a bland sense of smell. I have also heard of anecdotal evidence (including from readers of this blog) that depression leads to loss of fine sensation capabilities in other realms too including loss of an ability to discern pitch. Thus, to me it seems that the reason one has bland sensations in depressive states may have to do with reduced neurogeneisis and loss of neurons in the sensory areas. Anti-depressants also restore the sense acuity back, so apparently they are able to induce neurogenisis and plasticity in other barin regions than the hippocampus and their anti-depressant effects may largely be due to this factor. I had hypothesized earlier that depressed people should have diminished sense in other areas too – like that of vision and it will be interesting to see if data exists to support this view. Are there disorders similar to the ‘lazy eye’ that are more common in depressed people than in normal controls ; if so they would definitely be cured by prozac and one reason why people may be getting better due to medication may be because they can feel the world as vivid again. I theorize that while everything seems more vivid in mania, the reverse is true for depression and the underlying reason may be the anomalous neurogenesis. If so, there is hope for people who get their senses diminished as a result of depression- with an insight into how anti-depressants work – by improving neurogenisis and plasticity- we may be able to make better drugs that benefit them.
I’ll be watching this anti-depressant as a general enhancer of plasticity theory very keenly in the future and would love any pointers to research on the same lines from my readers.
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Depression, Dreaming and Rehearsal learning
Jan 7th
We all know that depression is marked by an increase in REM Sleep or dreaming and their are various theories of why this increased dreaming may be a root cause of depression itself. One theory posits that having too much dreams or emotional negativity even while sleeping (most dreams have negative content) may lead to maintenance of downward spiral of depressive cognitive and emotional style. Another theory posits that having too much negative dreams may lead us to get exhausted and the morning weariness found in depression is due to this fact.
I’ll not comment regarding the purported mechanism and causal direction of link between depression and dreaming. Suffice it to note few pertinent facts:
- Depressives dream 3 -4 times more than normal people.
- Most Anti-depressants cause REM sleep to be suppressed and this may underlie their therapeutic action or may just be a side-effect.
- There is mixed evidence as to whether REM sleep is also altered in Mania (although a decrease in REM sleep is not mentioned in literature- if anything REM increases just like in depression)
Now I’ll like to highlight an important experiment conducted by Wisconsin Madison scientists. They deprived rats of REM sleep and found that such rats became idiots in terms of survival sense and failed all standard test of survival. I’ll first describe the procedure and their results and then theorize:
What happens when a rat stops dreaming? In 2004, researchers at the University of Wisconsin at Madison decided to find out. Their method was simple, if a bit devilish. Step 1: Strand a rat in a tub of water. In the center of this tiny sea, allot the creature its own little desert island in the form of an inverted flowerpot. The rat can swim around as much as it pleases, but come nightfall, if it wants any sleep, it has to clamber up and stretch itself across the flowerpot, its belly sagging over the drainage hole.
In this uncomfortable position, the rat is able to rest and eventually fall asleep. But as soon as the animal hits REM sleep, the muscular paralysis that accompanies this stage of vivid dreaming causes its body to slacken. The rat slips through the hole and gets dunked in the water. The surprised rat is then free to crawl back onto the pot, lick the drops off its paws, and go back to sleep—but it won’t get any REM sleep.
Step 2: After several mostly dreamless nights, the creature is subjected to a virtual decathlon of physical ordeals designed to test its survival behaviors. Every rat is born with a set of instinctive reactions to threatening situations. These behaviors don’t have to be learned; they’re natural defenses—useful responses accrued over millennia of rat society.
The dream-deprived rats flubbed each of the tasks. When plopped down in a wide-open field, they did not scurry to the safety of a more sheltered area; instead, they recklessly wandered around exposed areas. When shocked, they paused briefly and then went about their business, rather than freezing in their tracks the way normal rats do. When confronted with a foreign object in their burrow, they did not bury it; instead, they groomed themselves. Had the animals been out in the wild, they would have made easy prey.
The surprise came during Step 3. Each rat was given amphetamines and tested again; nothing changed. If failure to be an effective rat were due to mere sleep deprivation, amphetamines would have reversed the effect. But that didn’t happen. These rats weren’t floundering because they were sleepy. Something else was going on—but what?
To me it seems that what is happening in these dream-deprived rats is an unlearning of learned helplessness paradigm. In learned helplessness, one stops exploring the environment and becomes extremely cautious. Learned helplessness is an extremely influential theory of depression and I have blogged about it previously. In the dream-deprived rats something exactly the opposite is happening – they are becoming more exploratory and sort of unlearning the basic survival instincts .
To me all this seems to nicely fit together. Dreams may be instrumental in rehearsal learning and when the rat (or human) has been repeatedly exposed to inescapable shocks (unavoidable stress), then it may lose the desire to explore not only in the real world, but also in the dream world – the primary purpose of which is to generate alternative strategies to previously un-encountered negative situations. When one loses or fails to find creative solutions to the inescapable situations, one falls in a negative dream loop whereby one fails to explore adequately new strategies or to reassess the environment in light of new evidences. Instead as one has failed to find creative solutions earlier, one;s dreams become pre-occupied with failure- and with each failure prompts more vigorous search for answers in the dream -thus leading to more REM sleep. Also, as REM sleep is required for thus maintaining the new (unhealthy) associations hence as long as adequate REM sleep is available one stays stuck with the learned negative associations and the learned helplessness.
SSRIs and other anti-depressants , by blocking the REM sleep , may be providing one additional step whereby dreaming stops for some duration and the synapses that underlie negative associations (that were constantly strengthened during dreams) are given time to naturally become weak. Thus events no longer have automatic negative connotations, but can be appraised afresh with a new outlook. This may be one putative mechanism of how anti-depressants work. This may also explain why anti-depressants take so much time to become effective. When dreaming stops, the unlearning doesn’t happen in a day- the weakening of associations would take weeks and months to materialize and have an effect.
Cognitive – behavioral theory may also be working on the level of dreams and it would be interesting to note how much dreaming is reduced and brought to normal levels as CBT starts showing effects.
The behavior of the dream deprived rat seems almost manic- unconcerned with survival and unnecessarily risk-taking. One experiment that can be conducted is to first induce learned helplessness in rats (by exposing them to unavoidable shocks) and then dream-deprive them as per the above methodology. If dream-deprivation restores the normalcy in rats and removes the depressive symptomatology we have a new theory of how depression works. This is not a difficult experiment to do and can be easily performed. I’m sure it will lead to positive results. I look forward to hearing from some readers of this blog as to how the experiment actually went (I myself am in no position to conduct such experiments). Do let me know via comments the experimental results- even if they are negative.
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