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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 10 of 10. This is the beginning of the thread.
Posted by cumulative on August 27, 2007, at 23:49:26
I'm on the 6mg EMSAM patch, soon to bump it to 9mg. School starts mid-september, upon which I will add transdermal nicotine.
This is with an aim healing my severe inattention moreso than any mild mood problems -- I do not tolerate traditional stimulants well and I believe that this combination may be useful. Nicotine has shown efficacy in ADD, and some people report EMSAM might be useful here as well. Improved dopaminergic function? I hope so.
http://dr-bob.org/babble/20061206/msgs/711818.html
I am not worried about tolerance/dependency from the nicotine, the psychologically addictive potential of which is considered to be very low in transdermal form. Low reinforcement. To deal with physical tolerance I will be tapering down at the end of every three-month semester -- perhaps restarting when the next semester comes if all has gone well.
I'd like to keep a log of this, and I'll keep people updated on efficacy.
It's a bit early, but anyone have any initial thoughts?
Posted by Quintal on August 28, 2007, at 0:24:52
In reply to EMSAM with transdermal nicotine for ADD control., posted by cumulative on August 27, 2007, at 23:49:26
I'm interested in nicotine for ADD and depression too. I've noticed that when I withdrawal from opiates suddenly I'll start craving cigarettes (dopamine?) and I've been wondering what effect it would have. I'd be very interested to see how you respond. Are you a smoker?
Q
Posted by cumulative on August 28, 2007, at 23:37:02
In reply to Re: EMSAM with transdermal nicotine for ADD contro » cumulative, posted by Quintal on August 28, 2007, at 0:24:52
Not a smoker. I've been using gum on and off with not much effect besides nausea if I keep it in my mouth too long, but my hopes are still high. I've responded decently to patches in the past.
Tolerance could definitely be an issue. Someone told me, though, that nicotine will activate stimulant reverse tolerance for dopamine. There haven't really been any long-term studies on the effectiveness of the stuff for ADD/ADHD, I think.
Cost: Cost is high. Now, in a brilliant marketing stroke the high-dose patches cost the same as the low-dose patches, so I might just buy 21mg patches in bulk and cut them for a while. I hear though that this can expose the patches to air and destroy some of the nicotine, but maybe there's a way to properly store the cut patches so this doesn't occur?
What might be useful is an elucidation of some more of the neurochemistry of nicotine.
Can someone explain the functional differences to me between an acetylcholinesterase inhibitor and nicotine, which stimulates nicotinic acetylcholine receptors (causing downstream release of catecholamines)? Am I getting more acetylcholine activity, or is (as one person said I think) the nicotinic acetylcholine receptor actually opposed in some ways to regular ACh ...?
Here's hoping it works. If it doesn't, I'll probably be f*cking up a class I'm really looking forward to, and maybe another six months of not really connecting with people at my new school. If it doesn't work, next step might be the Daytrana patch ... plus aricept.
Posted by linkadge on August 29, 2007, at 9:40:05
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by cumulative on August 28, 2007, at 23:37:02
In terms of tollerance, I don't think one will gain tollerance to all the effects.
I read an article that said that unlike other stimulants, nicotine acutally increased the expression of the d3 receptors in the neucleus accumbens over time.
This is similar to the effects of repeated antidepressant treatments such as amitryptaline, parnate etc.
Linkadge
Posted by Quintal on August 29, 2007, at 9:58:37
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by cumulative on August 28, 2007, at 23:37:02
>Tolerance could definitely be an issue. Someone told me, though, that nicotine will activate stimulant reverse tolerance for dopamine.
Yeah, according to Wiki, nicotine seems to be one of the few substances that induces reverse tolerance.
____________________________________________________In many studies it has been shown to be more addictive than cocaine and heroin, though chronic treatment has an opposite effect on reward thresholds. Like other physically addictive drugs, nicotine causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. In addition, the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. The net effect is an increase in reward pathway sensitivity, opposite of other drugs of abuse (namely cocaine and heroin, which reduces reward pathway sensitivity). This neuronal brain alteration persists for months after administration ceases. Due to an increase in reward pathway sensitivity, nicotine withdrawal is relatively mild compared to ethanol or heroin withdrawal. Also like other highly addictive drugs, nicotine is addictive to many animals besides humans. Mice will self-administer nicotine and experience behavioral unpleasantries when its administration is stopped. Gorillas have learned to smoke cigarettes by watching humans, and have similar difficulty quitting.
http://en.wikipedia.org/wiki/Nicotine#Dependence
--------------------------------------------------Research suggests that when smokers wish to achieve a stimulating effect, they take short quick puffs, which produces a low level of blood nicotine. This stimulates nerve transmission. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, Nicotine potently enhances the actions of norepinephrine and dopamine in the brain causing a drug effect typical of pyschostimulants. At higher doses nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use.
Nicotine gum and patches are available, usually in 2 mg or 4 mg doses of gum, that do not have all the other ingredients in smoked tobacco. They appear to be not as addictive or as pleasurable, and perhaps have fewer side effects [citation needed]. Whether all the other psychoactive effects also occur has not been well studied.
http://en.wikipedia.org/wiki/Nicotine#Psychoactive_Effects
__________________________________________________Q
Posted by linkadge on August 29, 2007, at 13:11:35
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by Quintal on August 29, 2007, at 9:58:37
Unlike most drugs of abuse though, most smokers reach a certain number of smoked cigarettes and then generally don't compulsivly increase.
The monoamine oxidase inhibiton too may affect the way that the brain adapts to nicotine.
Some studies suggest that smokers increase till they find a desired level of monoamine oxidase ihibition, not nicotine bloodlevel.
Linkadge
Posted by Quintal on August 29, 2007, at 14:45:10
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by linkadge on August 29, 2007, at 13:11:35
Posted by cumulative on August 29, 2007, at 15:09:01
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by Quintal on August 29, 2007, at 9:58:37
That's interesting. It's funny though, I've heard the multiplication of acetylcholine receptors as being somewhat responsible for withdrawal unpleasantness -- now, wouldn't this indicate that nicotine is calming non-nicotinic acetylcholine?
re: stimulant reverse tolerance, I certainly hope so. If this works out for me, I'll be posting a full report. My use of EMSAM for full MAO-A/MAO-B is perhaps a wrench in the works -- anyway I'll see what happens.
Linkadge: you're very knowledgeable ... let me ask you about latent inhibition. Many dopaminergics seem to lower latent inhibition (amphetamine seems to abolish it). Nicotine lowers it in some studies, increases it in some studies, and smokers seem to have a generally increased amount of it. What do you make of all this?
Posted by Quintal on August 29, 2007, at 15:57:58
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by cumulative on August 29, 2007, at 15:09:01
>That's interesting. It's funny though, I've heard the multiplication of acetylcholine receptors as being somewhat responsible for withdrawal unpleasantness -- now, wouldn't this indicate that nicotine is calming non-nicotinic acetylcholine?
I've no idea off the top of my head :-) I just took a Xanax and my mind is wandering. All that keeps running through my mind is galantamine. Forgotten what it is. Does something to these things >nicotinic acetylcholine receptors<. Was thinking of trying it as an alternative to nicotine but it was too hard to find one that shipped to the UK and accepted my debit card. Do benzos have any effect on latent inhibition?
Q
Posted by linkadge on August 29, 2007, at 20:09:58
In reply to Re: EMSAM with transdermal nicotine for ADD contro, posted by cumulative on August 29, 2007, at 15:09:01
When stimulants work for ADHD they typically increase the ability of the individual to disregard irrelavant stimulii. If they are used in high doses, or doses required to get high, I believe the opposite can happen, ie they can greatly increase the contious awareness of otherwise irrelavant stimulii.
Nicotine shows some efficacy as an ADHD treatment on its ability to decrease distractability. Typically, a correct amount dopaminergic activity in the frontal cortex produces inhibition in other brain regions, too much or too little will alter latent inhition.
Unlike other stimulants, nicotine can modulate serotonergic firing in the dorsal raphai neucleus (kind of like the anxiolyic buspar), by modulating presynaptic serotonin autoreceptor function. This can reducing anxiety, and also help to decrease internal "background noise". It can be good for "mind noise" for this reason.
I think the propensity of stimulants to lower latent inhibition is also "disease dependant".
For instance, in schizphrenia, a stimulant may significantly increase the distractability, disturbed thought processes, and produce an overall cognative deterioration. It may make the individual *less* able to filter out irrelavant environmental stimuli. In such cases a stimulant would probably be lowering latent inhition.
For a person with ADHD, the stimulant generally increases the persons ability to filer out irrelavant environemental materials thus increasing latent inhibiton.
That would just be my speculation. The notion that stimulants lower latent inhibition probably also applies to when stimulants are abused in high enough that can cause psychosis etc.
Linkadge
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