![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 14 to 38 of 38. Go back in thread:
Posted by Think1234 on June 10, 2006, at 19:14:25
In reply to Klonopin is a Paradoxical Stimulant, posted by Think1234 on June 10, 2006, at 18:40:46
Actually Klonopins actions on the Amygdala are usualy less direct than I explained in the previous post. Glutamate cells, which produce the neurotransmitter Glutamate act directly on the Amygdala. Konopin depresseses the actions of the Glutamate and thus depresses the action of the Gaba within the Amygdala. Generally P-docs use the term paradoxical stimulant when talking about, exacerbated anxiety, aggressiveness, argumentativeness, etc which sometimes occur with the use of klonopin. When I refer to klonopin as a paradoxical stimulant I mean that its is brake for the brains brake (the amygdala). Which makes klonopin, in a sense, a stimulant.
This quote explains the actions of Benzodiazepines from an even more complex perspective than either of my explanation of
klonopins actions.
"Don’t Ask, Don’t Tell, but Benzodiazepines
Are Still the Leading Treatments for Anxiety Disorder"
Stephen M. Stahl, M.D., Ph.D
www.psychiatrist.com/brainstorms/br6309.pdf"The amygdala apparently acts as
the brain’s panic button. Push it hard
enough with emotional input from
any of several areas of the brain, and it
will trigger an alarm of fear via mul-
tiple brain pathways connecting to the
body. Some inputs to the amygdala
are fast and precipitate fear reactions
that occur like a reflex and without
thought. Other inputs are detoured
momentarily to the cortex and hip-
pocampus where they are analyzed
before the decision is made to hit the
panic button. Emotional inputs to the
amygdala frequently use the excita-
tory neurotransmitter glutamate to
ring the alarm, but triggering of the
alarm by glutamate can be tempered
by both GABA and serotonin.Gaba interneurons in the cortex and hip-
pocampus inhibit emotional input to
the amygdala, as do serotonergic
nerve terminals from the raphe.
GABA interneurons and serotonergic
nerve terminals in the amygdala itself
act as potential brakes on amygdala
output to the fear response. Thus,
agents that boost output from either
GABA or serotonin neurons each
have at least 2 chances—from both
outside and inside the amygdala—
to diminish the likelihood of anxiety
and fear."
Posted by Think1234 on June 10, 2006, at 19:33:04
In reply to Klonopin's = stimulant/ includes quoted source., posted by Think1234 on June 10, 2006, at 19:14:25
To understand klonopins relationship to serotonin. Just read my second post. It will include a quote that explains the serotonergic effects of Klonopin. Basically Klonopin inhibits serotonin cells which activate the amygdala.
But that of course is only part of the story. And like many drugs in psychiatry or an other medical field, the theory doesn't always match the reality.
Posted by cecilia on June 10, 2006, at 20:51:08
In reply to Re: Klonopin Mechanisms? (long), posted by willyee on June 10, 2006, at 17:00:33
It's fine for them to say that clonazepam should be used in conjunction with a successful anti-depressant. Unfortunately, a lot of us have never found such a thing. Cecilia
Posted by zeugma on June 11, 2006, at 6:47:59
In reply to Klonopins relationship to serotonin, posted by Think1234 on June 10, 2006, at 19:33:04
you mean, Klonopin inhibits glutamate via a GABA effect, similar to the way serotonin inhibits glutamate excitation of the amygdala.
Alcohol is a paradoxical stimulant because it activates serotonin-3 receptors which increase dopamine release in the ventral tegmental area. This is why alcohol improved my ADD symptoms, although this was not a practical long-term treatment at all. Alcohol was a more successful, though short-acting and side-effect-ridden, treatment for my ADD than for my anxiety.
-z
Posted by Squiggles on June 11, 2006, at 7:00:24
In reply to Re: Klonopins relationship to serotonin » Think1234, posted by zeugma on June 11, 2006, at 6:47:59
I don't think there's anything paradoxical
at all about any of these drugs. Think
about the meaning of "paradoxical". What
does it mean in terms of clinical response?
It means that you get responses which are
unexpected or unpredicted. That's pretty
vague. You can get paradoxical effects
with aspirin if you take it on an empty
stomach for example.In the case of benzos, alcohol, Klonopin
whatever -- paradoxical may mean that
there is a time variable in the metabolism
of the drug.It's not an inherent quality of the drug
itself.Squiggles
Posted by SLS on June 11, 2006, at 7:19:30
In reply to Klonopin is a Paradoxical Stimulant, posted by Think1234 on June 10, 2006, at 18:40:46
I think the phenomenon known as disinhibition can act to create an excitable behavioral state under the influence of both BZDs and alcohol.
Zeugma: I didn't know that alcohol acted on 5-HT3 receptors. How does that work?
- Scott
Posted by SLS on June 11, 2006, at 7:53:47
In reply to Re: Klonopins relationship to serotonin » Think1234, posted by zeugma on June 11, 2006, at 6:47:59
Hi Z.
I think I'll pick your brains, if you don't mind. Mine isn't working too well these days. You know, I'm almost afraid to say anything because I know it could be so much worse.
Does the ventral tegmental area have projections efferent or afferent to the dorsolateral prefrontal cortex? Where does the VTA lie relative to the nucleus accumbens and DLPFC?
Thanks. I'm trying to understand why antidepressants poop out on me so quickly. What kind of feedback mechanism is causing this to happen? My brain refuses to accept change.
- Scott
Posted by zeugma on June 11, 2006, at 10:22:53
In reply to Re: Klonopins relationship to serotonin » zeugma, posted by SLS on June 11, 2006, at 7:53:47
Hi Scott.
The VTA has projections afferent to the entire PFC (the "mesocortical" pathway). It also projects to the striatum (the "Mesolimbic" pathway). There is also a "mesocoerulear" pathway to the locus coeruleus affecting the NE system.
The VTA, like the LC, is in the brain stem.
The accumbens is next door to the amygdala, and both are posterior to, and below, the cortex.
I wish I knew why AD's poop out so rapidly for you. Why do you think the DLPFC is involved?
-z
Posted by SLS on June 11, 2006, at 11:46:14
In reply to Re: Klonopins relationship to serotonin » SLS, posted by zeugma on June 11, 2006, at 10:22:53
Thanks for replying, Zeugma.
> The VTA has projections afferent to the entire PFC (the "mesocortical" pathway). It also projects to the striatum (the "Mesolimbic" pathway). There is also a "mesocoerulear" pathway to the locus coeruleus affecting the NE system.
>
> The VTA, like the LC, is in the brain stem.
>
> The accumbens is next door to the amygdala, and both are posterior to, and below, the cortex.
>
> I wish I knew why AD's poop out so rapidly for you. Why do you think the DLPFC is involved?
Because of how cognitively affected and mentally slowed I am. I have almost no short-term memory. It is as if my executive functions have been dampened or poorly stimulated. I also display a "deficit syndrome" that probably involves hypoactiviy in limbic areas. I was wondering if there were hypoactive limbic afferents to the DLPFC that might not be stimulating that area enough. Perhaps it is the other way around. Maybe a hypoactive DLPFC fails to stimulate reward centers. Maybe deficiencies in the LC fail to stimulate the DLPFC directly or indirectly.Which comes first, the chicken or the egg?
Contrary to how I might appear in my writing, I literally cannot read beyond 2 or 3 sentences. Long paragraphs are overwhelming, and I must resort to skimming.
- Scott
Posted by ed_uk on June 11, 2006, at 13:50:40
In reply to Re: Klonopin Mechanisms? » willyee, posted by Squiggles on June 9, 2006, at 19:34:10
Hi
Clonazepam is available in the UK, but is used mainly as an anti-convulsant. The brand name is Rivotril.
Ed
Posted by zeugma on June 11, 2006, at 14:50:25
In reply to Re: Klonopins relationship to serotonin » zeugma, posted by SLS on June 11, 2006, at 11:46:14
Because of how cognitively affected and mentally slowed I am. I have almost no short-term memory. It is as if my executive functions have been dampened or poorly stimulated. I also display a "deficit syndrome" that probably involves hypoactiviy in limbic areas. I was wondering if there were hypoactive limbic afferents to the DLPFC that might not be stimulating that area enough. Perhaps it is the other way around. Maybe a hypoactive DLPFC fails to stimulate reward centers. Maybe deficiencies in the LC fail to stimulate the DLPFC directly or indirectly.>>
The DLPFC has a particular connection with spatial memory, and DLPFC lesions compromise performance on any task that requires maintainance of spatial information (for example, humans with DLPFC lesions would be unable to find their way through an airport). The DLPFC is also, as you know, deactivated during REM sleep, and dreams are processes in which one 'loses one's way.' (It is a selective deactivation because the other areas of the cortex are still active, although without NE or 5-HT inputs.) Of the various drugs I have taken, modafinil most strongly activates the 'dorsal pathway,' which is involved in determining where an object is. Methylphenidate by contrast is best for various forms of agnosia, such as a difficulty with facial recognition and difficulty perceiving colors: this is the 'ventral' pathway (determining 'what' an object is). Of note, methylphenidate is MUCH better with anhedonia and other 'negative' symptoms (the striatum is ventral to the PFC). I am only speaking of my own experience though it tallies with the literature.
The problem with all this is that researchers are able to report on the effects of particular lesions or manipulations of neurotransmitters, but the interactions between all the systems are not known, although manipulating one system produces change in all.
I'm not sure if any of this is helpful. The formula I have here in front of me- that striatal D2 stimulation produces cognitive flexibilty, while PFC D1 stimulation produces cognitive stability- seems far too simple. What do you think?
-z
Posted by Squiggles on June 11, 2006, at 15:31:47
In reply to Re: Klonopin Mechanisms? » Squiggles, posted by ed_uk on June 11, 2006, at 13:50:40
> Hi
>
> Clonazepam is available in the UK, but is used mainly as an anti-convulsant. The brand name is Rivotril.
>
> EdIt has many trade names. "Rivotril" is
one of them. So, what do they know about
it in the UK that they don't in Canada
and the US?Squiggles
Posted by Think1234 on June 11, 2006, at 16:34:28
In reply to Re: Klonopins relationship to serotonin » Think1234, posted by zeugma on June 11, 2006, at 6:47:59
" you mean, Klonopin inhibits glutamate via a GABA effect"
I believe thats what I said.
"similar to the way serotonin inhibits glutamate excitation of the amygdala."
Thank you for informing me of this."Alcohol is a paradoxical stimulant because it activates serotonin-3 receptors which increase dopamine release in the ventral tegmental area. This is why alcohol improved my ADD symptoms, although this was not a practical long-term treatment at all. Alcohol was a more successful, though short-acting and side-effect-ridden, treatment for my ADD than for my anxiety."
Thats news to me. I'm glad you found at least something. Remember that alcohol's actions are not fully known. The amygdala does indeed play are role in alcohols anxiolytic/stimulant effect via frontal efferent disinhibition.
Posted by ed_uk on June 11, 2006, at 16:52:10
In reply to Re: Klonopin Mechanisms? » ed_uk, posted by Squiggles on June 11, 2006, at 15:31:47
>It has many trade names. "Rivotril" is one of them.
Yeah, I was just saying that the brand name is Rivotril in the UK, since your earlier post implied that clonazepam wasn't available in the UK.
>So, what do they know about it in the UK that they don't in Canada and the US?
Nothing. Roche initially marketed several benzos for anxiety eg. Librium and Valium. They then introduced several benzos for sleep (eg. Mogadon) and epilepsy (eg. Rivotril). The various benzos have a lot in common. Roche decided to market numerous benzos for different uses because that way more people would end up taking benzos and they would make more profit. Rivotril is effective for both anxiety disorders and epilepsy. In the UK, it is approved only for epilepsy. If Roche had wanted, they could have got it approved for anxiety in the UK. I assume that they chose not to because they had already marketed several other anxiolytics in the UK.
Posted by RobertDavid on June 11, 2006, at 23:57:08
In reply to Re: Klonopin Mechanisms? » Squiggles, posted by ed_uk on June 11, 2006, at 16:52:10
I'll just say that klonopin was the best benzo I've tried for daily treatment of SAD and GAD. Key was getting to the right dose (2mgs at night).
Those that have not found an anti depressant that works for them to take with klonopin might consider taking provigil with it. Quite stimulating and does seem to improve mood for many.
Great thing about provigil is you know right away if you feel better vs waiting a month or two. By night time the stimulation eases and you can get some sleep. Just a thought.
Posted by Squiggles on June 12, 2006, at 7:43:19
In reply to Re: Klonopin Mechanisms?, posted by RobertDavid on June 11, 2006, at 23:57:08
> I'll just say that klonopin was the best benzo I've tried for daily treatment of SAD and GAD. Key was getting to the right dose (2mgs at night).
>
> Those that have not found an anti depressant that works for them to take with klonopin might consider taking provigil with it. Quite stimulating and does seem to improve mood for many.
>
> Great thing about provigil is you know right away if you feel better vs waiting a month or two. By night time the stimulation eases and you can get some sleep. Just a thought.
That sounds very helpful. I'll have to look up
povigil and see if it is strong enough to
compete with the tricyclics for major depression
(for my friend). As for the adjunt benzo, it
does seem that most antidepressants (probably
not the atypical psychotics and lithium) produce
anxiety as a side effect. I think this is
especially so with the new SSRIs, from what
I have gleaned on the net and the recent discussion re: the FDA paper.Squiggles
Posted by SLS on June 12, 2006, at 10:42:16
In reply to Re: Klonopins relationship to serotonin » SLS, posted by zeugma on June 11, 2006, at 14:50:25
Hey Z.
> The problem with all this is that researchers are able to report on the effects of particular lesions or manipulations of neurotransmitters, but the interactions between all the systems are not known, although manipulating one system produces change in all.
>
> I'm not sure if any of this is helpful. The formula I have here in front of me- that striatal D2 stimulation produces cognitive flexibilty, while PFC D1 stimulation produces cognitive stability- seems far too simple. What do you think?You have indeed been helpful. I didn't realize how important the striatum was for cognition. I guess I'm trying to distinguish between the site of primary dysfunction and those areas that are affected as secondary.
Have you ever played with melatonin to help adjust your circadian rhythm?
- Scott
Posted by zeugma on June 12, 2006, at 18:12:19
In reply to Re: Klonopins relationship to serotonin » zeugma, posted by SLS on June 12, 2006, at 10:42:16
hey Scott.
>>>
I didn't realize how important the striatum was for cognition.>>A lot of the research that's been done of this nature has been conducted in Parkinson's disease patients, who suffer a progressive depletion of DA from the dorsal striatum, which connects with the dorsal PFC, to the ventral striatum, which connects to the ventral PFC- a.k.a. the orbitofrontal PFC, said to be problematic for bipolars, and excessive stimulation of which (through L-Dopa therapy) produces such problems of excessive DA activity as the well-known 'pathological gambling' syndrome. L-Dopa actually produces highly variable cognitive effects in patients, depending on how far into the striatum the disorder has progressed. In patients with excessive striatal activity, a drug such as sulpiride can actually have cognitive benefits.
>>
I guess I'm trying to distinguish between the site of primary dysfunction and those areas that are affected as secondary.
>>That is an entirely worthwhile goal. I wish I knew more about the circuitry, but since I don't, I'll quote a passage that seems like it might be fruitful. It's from Elkhonon Goldberg's book on the PFC, "The Executive Brain", and he gets very explicit about neurotransmitters and regions of the brain that he thinks important in various syndromes, though he presents it as the result of a highly speculative Russian tradition that is not part of Western common currency:
"According to them [scientists at the Bourdenko Institute of Neurosurgery in Moscow], L-Dopa...improves the functions we typically associate with the posterior aspect of left frontal lobe: motor sequencing, speech initiation, expressive language....By the same token L-Dopa seems to retard the functions commonly associated with the parietal lobes (spatial orientation and spatial construction). L-glutamic acid...improves... other functions associated with the frontal lobes. It imporves insight into one's condition (reduces symptoms of anosognia), improves the sense of humor [!], time estimation, and time sequencing. L-glutamic acid also improves the functions typically associated with the parietal lobes [assuming modafinil works on this structure, this is indeed true. Modafinil does indeed improve my comedic abilities {source of its AD effects IMO}, but the parietal lobe is also associated with the "dorsal" stream I referred to in my previous post. And how Russian, to mention sense of humor as a faculty worthy of notice by neurologists! I am of Russian descent]. L-tryptophan...improves the functions of the parietal lobe but retards the functions of the frontal lobes, particularly the functions of the left frontal lobe. Ameridin, an anticholinesterase not commonly known in the United States, seems to improve the functions of the parietal lobes, particulary the left parietal lobe. It improves comprehension of grammar..." (pp.195-196)
I find these Russian speculations fascinating to revisit after i have taken drugs that mimic the effect of some of these substances, and I find they are remarkably congruent with my own experience and what I know of the Western tradition of neuroscience. It also shows how delicate the balance is between neurotransmitters and structures, and this is something Trevor Robbins, who is my main source for information on DA and the fronto-striatal pathways, emphasizes: 'cognition enhancers' inevitably have 'cognitive side effects.'
>>
Have you ever played with melatonin to help adjust your circadian rhythm?
>>That is an interesting idea. melatonin seems to be similar in some ways to serotonergetic manipulations, in particular blockade of the 5-HT 2A/C receptors, and also to 5-HT 1A agonism:
Eur Neuropsychopharmacol. 2006 Mar 6; [Epub ahead of print]
Melatonin affects the immobility time of rats in the forced swim test: The role of serotonin neurotransmission.Micale V, Arezzi A, Rampello L, Drago F.
Department of Experimental and Clinical Pharmacology, University of Catania, Catania, Italy.
The efficacy of melatonin or its derivatives in depressive patients has been recently considered for clinical application. However, the evidence for its effect on experimental models of depression is not consolidated. Here, the effects of melatonin on the model of forced swim test (FST) paradigm were studied in male rats of the Wistar strain after acute intraperitoneal (i.p.) administration of 0.1, 0.5 or 1 mg/kg of the hormone. Melatonin at doses of 0.5 and 1 mg/kg, but not of 0.1 mg/kg, decreased the immobility of rats in the FST paradigm suggesting a possible antidepressant-like activity. The dose of 0.5 mg/kg appeared to be as potent as clomipramine 50 mg/kg in reducing the immobility time of rats in the FST paradigm. The effect of melatonin on immobility time of rats in the FST paradigm was abolished by the simultaneous injection of the non-selective melatonin antagonist, luzindole (0.25 mg/kg, subcutaneously). Similarly, administration of small quantities of serotonin (5-HT, 5 ng/1 mul) or of the 5-HT(2A)/5-HT(2C) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (2 ng/1 mul) injected into the amygdale totally suppressed the reduction of immobility time in the FST paradigm induced by melatonin 0.5 mg/kg. These results may suggest that effects of melatonin on the behavioral reaction of rats in the FST paradigm are due to an interaction of the hormone with central 5-HT neurotransmission.
J Pineal Res. 2002 Aug;33(1):14-9.
Melatonin potentiates 5-HT(1A) receptor activation in rat hypothalamus and results in hypothermia.Lin MT, Chuang JI.
Department of Medical Research, Chi-Mei Medical Center, Yung-Kang City, Tainan Hsien, Taiwan. mtlin@ym.edu.tw
Effects of melatonin on both thermoregulatory responses and hypothalamic serotonin release were assessed in unanesthetized rats at three different ambient temperatures (Ta). Systemic administration of melatonin (30-120 mg/kg, i.p) caused a decrease in both colonic temperature and hypothalamic serotonin (5-HT) release in rats at both Ta 8 and 22 degrees C. The hypothermia was brought about by a decrease in metabolic rate at Ta 8 degrees C, whereas at Ta 22 degrees C the hypothermia was produced by both a decrease in metabolic rate and an increase in cutaneous temperature. However, in the heat (Ta 31 degrees C), neither thermoregulatory responses nor hypothalamic 5-HT release was affected by the same amount of administered melatonin. The melatonin-induced hypothermia and decreased 5-HT release in the hypothalamus were attenuated by selective depletion of brain 5-HT produced by intracerebroventricular injection of 5,7-dihydroxytryptamine. Furthermore, the melatonin-induced hypothermia was almost completely abolished by treatment with a 5-HT2A receptor agonist (DOI) or a 5-HT1A receptor antagonist [(-)-pindolol]. The data indicate that melatonin potentiates the 5-HT1A receptor activation in the hypothalamus and results in hypothermic effects which can be antagonized by the expected hyperthermic effect of DOI.
>>
The sleep docs I saw advocated Xyrem, however my pdoc is I think rightly reluctant to try that prematurely. My circadian rhythms have always been dysregulated. I will see if melatonin has interactions with any of the meds I'm taking.
I value your conversation and insights greatly.
-z
Posted by SLS on June 13, 2006, at 7:26:14
In reply to Re: Klonopins relationship to serotonin » SLS, posted by zeugma on June 12, 2006, at 18:12:19
Hi Z.
I can hardly that believe you took the time to type out that passage! Thank you.
> I value your conversation and insights greatly.
Likewise.
:-)
- Scott
Posted by ZeitGuest on June 13, 2006, at 16:43:00
In reply to Re: Klonopins relationship to serotonin » SLS, posted by zeugma on June 12, 2006, at 18:12:19
Which medications and/or supplements can one take to boost L-glutamic acid in the brain? You mention modafinil. Are there any others?
>>
L-glutamic acid...improves... other functions associated with the frontal lobes. It imporves insight into one's condition (reduces symptoms of anosognia), improves the sense of humor [!], time estimation, and time sequencing. L-glutamic acid also improves the functions typically associated with the parietal lobes
>>
Posted by zeugma on June 14, 2006, at 18:36:17
In reply to Re: Klonopins relationship to serotonin, posted by ZeitGuest on June 13, 2006, at 16:43:00
Which medications and/or supplements can one take to boost L-glutamic acid in the brain? You mention modafinil. Are there any others?>>
I'm sure someone has the answers to your question about supplements on the Alternative board.
As for glutaminergic drugs, there are a number of AMPA receptor potentiators in the pipeline, which are said to be very similar to modafinil in effect.
-z
Posted by zeugma on June 27, 2006, at 6:07:45
In reply to Re: Klonopins relationship to serotonin » SLS, posted by zeugma on June 12, 2006, at 18:12:19
L-glutamic acid...improves... other functions associated with the frontal lobes. It imporves insight into one's condition (reduces symptoms of anosognia), improves the sense of humor [!]>>
apparently I was right about modafinil:
Sleep. 2006 Jun 1;29(6):841-7.
The effects of caffeine, dextroamphetamine, and modafinil on humor appreciation during sleep deprivation.
Killgore WD, McBride SA, Killgore DB, Balkin TJ.
Division of Neuroscience, Department of Behavioral Biology, Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA. william.d.killgore@us.army.milSTUDY OBJECTIVES: Sleep loss consistently impairs performance on measures of alertness, vigilance, and response speed, but its effects on higher-order executive functions are not well delineated. Similarly, whereas deficits in arousal and vigilance can be temporarily countered by the use of several different stimulant medications, it is not clear how these compounds affect complex cognitive processes in sleep-deprived individuals. DESIGN: We evaluated the effects of double-blind administration of 3 stimulant medications or placebo on the ability to appreciate humor in visual (cartoons) or verbal (headlines) stimuli presented on a computer screen following 49.5 hours of sleep deprivation. SETTING: In-residence sleep-laboratory facility at the Walter Reed Army Institute of Research. PARTICIPANTS: Fifty-four healthy adults (29 men, 24 women), ranging in age from 18 to 36 years. INTERVENTIONS: Each participant was randomly assigned to 1 of 3 stimulant medication groups, including caffeine, 600 mg, n = 12; modafinil, 400 mg, n = 11; dextroamphetamine, 20 mg, n = 16; or placebo, n = 14. MEASUREMENTS AND RESULTS: Humor appreciation for cartoon stimuli was enhanced by modafinil relative to both placebo and caffeine, but there was no effect of any stimulant medication on the appreciation of verbal humor during sleep loss. In contrast, all 3 stimulants improved psychomotor response speed, whereas only caffeine and dextroamphetamine improved ratings of subjective sleepiness. CONCLUSIONS: Findings suggest that, despite similar alerting and vigilance-promoting effects, these 3 compounds have significantly different effects on those highly complex cognitive abilities mediated by the pre-frontal cortex.>>
I can't believe anyone actually did this study. Subjective sleepiness is no fun though
-z
Posted by Squiggles on June 27, 2006, at 6:30:56
In reply to insight into modafinil's mechanisms from cartoons, posted by zeugma on June 27, 2006, at 6:07:45
Is this a study the Bush Administration
supported for sleep-deprived and grumpy
military personnel? Hey guys, lighten up,
it's only a war.Squiggles
Posted by zeugma on June 27, 2006, at 16:50:44
In reply to Re: insight into modafinil's mechanisms from carto » zeugma, posted by Squiggles on June 27, 2006, at 6:30:56
>
> Is this a study the Bush Administration
> supported for sleep-deprived and grumpy
> military personnel? Hey guys, lighten up,
> it's only a war.>>how right you are.
emphasis on the 'only.'
that qualifier notwithstanding, the only studies we will be seeing that aren't PR for the drug companies will be coming out of the armed forces' pharmaceutical division. The rest of the public sector is fast disappearing.
i wish i took the same pleasure in the exploits of cartoon heroes that certain members of our gov't do. that is assuredly the only heroism we will see out of them.
the study actually was in the great Russian/Soviet tradition of Luria, and suggests yet another parallel between U.S. 2006 and U.S.S.R. circa 1980.
-z
-z
>
> Squiggles
>
Posted by Dr. Bob on June 27, 2006, at 23:46:28
In reply to Re: insight into modafinil's mechanisms from carto » Squiggles, posted by zeugma on June 27, 2006, at 16:50:44
> Hey guys, lighten up,
> it's only a war.
>
> Squiggles> how right you are.
>
> emphasis on the 'only.'
>
> zeugmaPlease be sensitive to the feelings of others (such as those who consider the war a serious matter).
But please don't take this personally, this doesn't mean I don't like you or think you're bad people.
If you or others have questions about this or about posting policies in general, please first see the FAQ:
http://www.dr-bob.org/babble/faq.html#civil
http://www.dr-bob.org/babble/faq.html#enforceFollow-ups regarding these issues should be redirected to Psycho-Babble Administration -- and those regarding the war to Psycho-Babble Politics. They, as well as replies to the above posts, should of course themselves be civil.
Thanks,
Bob
This is the end of the thread.
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