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  #16  
Old 04-19-07, 09:10 AM
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Hmmm. Never felt that on any of mine, either. Cymbalta came close, but there's one particular pleasure it interferes with mightily, so it's far from perfect.

BTW, antidepressants do work on different chemicals. Paxil, Celexa, and I forget what else are primarily serotonin, but Wellbutrin works on dopamine and Effexor targets norepinephrine. All three are related to each other, and the SSRIs an SNRIs at the correct dose will become SSNRIs. Wellbutrin can be combined with SSRIS or SNRIs because it has minimal effect on serotonin and norepinephrine, but combining the other two types can cause some serious problems if they start boosting the absorption of each others' chemicals.
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Old 04-19-07, 05:06 PM
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Wellbutrin is more related to stimulants than it is to the other anti-depressants. In fact, I would bet that the only reason why it isn't a scheduled drug (schedule II in fact) is because the seizure threshold is very low, making it a hard to abuse drug. Perhaps that is where the original idea of anti-depressants giving "overwhelming pleasure" (though I still think those words are stretching it).

Oh, and Effexor primarily targets Serotonin, secondarily targets Norepinephrine (at fairly high doses), and targets Dopamine (at a significant enought affinity to even mention anyway) at very high doses. I believe Cymbalta is more balanced in the Serotonin vs. Norepinephrine. Tricyclics are often biased torwards Norepinephrine (especially in the case of Desipramine).
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Old 04-21-07, 07:20 PM
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Before I get my responses to the three thread's I am currently engaged in I guess I should begin posting my findings. . . . some times I do get the responses mixed up resulting in an appears of incoherence on my behalf.


Quote:
Originally Posted by faylen
I know that there are illegal recreational drugs out there that can permanently disable the receptors for serotonin, and I'd imagine that a lot of these neurological conditions involve receptor damage, so no matter how much of a medication you're given, nothing will change. Add in individual body chemistry and workings, and you have even more variables. Plus, the brain is only recently being effectively mapped, and its complexity is pretty daunting. Most of what neurobiologists are doing for people with depression, ADD, autism, schizophrenia, and so on is like a game of darts.
Actually we may metabolize medications differently which may also account for differences, then there is already present body chemistry however there is a little more reasoning behind doctors choices than simple guess work.

Here is a good simplified over view of which drugs effect what neurotransmitters

THE CHEMISTRY OF EMOTIONS
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  #19  
Old 04-21-07, 08:20 PM
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i think that norepinephrine is responsible for attention, alertness, and energy for attention.....dopamine is the rewarding feeling of paying attention and motivation

I think people with inattentive ADD, assuming 100 points is the max norm for both epinephrine and dopamine, we have like 35 points dopamine and 25 points epinephrine

after medication our levels balance out to a normal person....so when we are paying attention in class or in conversation our dopamine levels go up to 60 points and our epinephrine levels go up to 80 points instead of staying at 35 and 25

dopamine is still very important because the rise in norepinephrine for energy to pay attention, stay stabily focused, and take things seriously has to be balanced with feel good, motivating dopamine so that it won't feel like you are running away from guy with a knife

but........norepinephrine is usually enough......but the average person feels better then us because of their extra dopamine when paying attention, listening, and comprehending thus why we shouldn't settle for just increase in norepinephrine

just norepinephrine is good for when playing a sport in which we lack of it...............because the norepinephrine and the following adrenaline we should be getting is needed to keep playing aggresive and take the game seriously
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Old 04-22-07, 01:34 AM
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Do they really know?

Dig this stuff here.

The influence of methylphenidate on the power spectrum of ADHD children – an MEG study


Clarke and colleagues [17-19] investigated cortical differences between ADHD children of the combined type (ADHDcom) and the predominantly inattentive type (ADHDin). Generally, they found ADHDcom children having higher slow wave activity than ADHDin children. The authors concluded from their results that children with ADHDcom are more cortically hypoaroused than children with ADHDin. They hypothesized that ADHDcom might be related to frontal lobe dysfunctions, while children with ADHDin may have other forms of CNS functioning.

Due to the findings that MPH is more effective for some children than for others and since the cortical profiles of ADHD subtypes seem to differ, it is advisable to study the effects of MPH on cortical processing more closely***End Quote


~Bold mine~


PLease note in the below study ADHD is used to describe ADD combined and ADD predominantly hyperactive although they pretty much are focusing on combined ADD type saying predomenantly Hyper active ADD is rare after six years old {Boy do I how wrong that is but it sould serve to communicate the point I was making which was. . .. . . the difference between subtypes. }

Attention-deficit disorder (attention-deficit/hyperactivity disorder without hyperactivity): A neurobiologically and behaviorally distinct disorder from attention-deficit/hyperactivity disorder (with hyperactivity)


ADD and ADHD That Includes Hyperactivity Are Dissociable Disorders
Whereas children with ADHD are frenetic and hyperactive, a significant proportion of children with ADD are exactly the opposite. A significant subset of children with ADD are hypoactive, sluggish, and very slow to respond (see Table 1). Children with ADHD are often insufficiently self-conscious; children with ADD tend to be overly self-conscious

Because of their disruptive behavior, children with ADHD are more likely to be suspended or expelled from school (Weiss et al., 2003). Conduct disorder and aggressivity are far more commonly comorbid with ADHD than with ADD (e.g., Barkley et al., 1990; Barkley, DuPaul, & McMurray, 1991; Faraone, Biederman, Wever, & Russell, 1998; Edelbrock, Costello, & Kessler, 1984; Goodyear & Hynd, 1992; Lahey et al., 1987; Morgan, Hynd, Riccio, & Hall, 1996; Nigg, 2000; Weiss et al., 2003). Conversely, children with ADD are somewhat more prone to internalizing disorders such as anxiety or depression (or at least show a marked absence of externalizing disorders) and tend to be more socially isolated or withdrawn than are children with ADHD (Barkley et al., 1990, 1991; Faraone, Biederman, Wever, & Russell, 1998; Edelbrock, Costello, & Kessler, 1984; Goodyear & Hynd, 1992; Lahey et al., 1987; Morgan, Hynd, Riccio, & Hall, 1996; Nigg, 2000; Weiss et al., 2003). Reading and language deficits are more commonly comorbid with ADD than with ADHD (Faraone et al., 1998; Warner–Rogers, Taylor, Taylor, & Sandberg, 2000; Weiss et al., 2003; Willcutt & Pennington, 2000) as are problems with mental mathematical calculations (Carlson, Lahey, & Neeper, 1986; Hynd et al., 1991; Marshall, Hynd, Handwerk, & Hall, 1997; Morgan et al., 1996).

Most children with ADHD (perhaps as high as 90%; Barkley, 2001; Barkley et al., 1991; Milich et al., 2001; Weiss et al., 2003) respond positively to methylphenidate (Ritalin) and over two-thirds of such children respond positively to methylphenidate in moderate to high doses (Barkley, 2001; Barkley et al., 1991; Milich et al., 2001; Weiss et al., 2003). In contrast, a significant percentage of children with ADD are not helped by methylphenidate and those who are helped often do best at low doses (Barkley, 2001; Barkley et al., 1991; Milich et al., 2001; Weiss et al., 2003). Many individuals with ADD are helped by amphetamines, such as Adderall. There is considerable overlap in the mechanisms of action of methylphenidate and amphetamines, but there is a significant difference. Although both methylphenidate and amphetamines inhibit reuptake of dopamine and norepinephrine, only amphetamines also promote release of those neurotransmitters. Recent research also suggests that low doses of methylphenidate (the dosages likely to be efficacious in treating ADD) preferentially release norepinephrine in the rat brain (Ishimatsu, Kidani, Tsuda, & Akasu, 2002). Possible problems with the neural release of norepinephrine in ADD are relevant to motivational issues discussed later.

{Although I will add I am primarily hyperactive and I respond better to Adderall than Ritalin - low does waste of my time basically making me sleepy}

Dopamine transporter (DAT) is the principal mechanism for reuptake of released dopamine. DAT is abundant in the striatum (Garris & Wightman 1994), where it is widely distributed and strategically located (Sesack, Hawrylak, Matus, Guido, & Levey, 1998). It is far less abundant and less well situated in the prefrontal cortex (Sanchez–Gonzalez & Cavada, 2003; Sesack et al., 1998). Hence, it plays a more important role in striatal function than in prefrontal function. DAT is the product of the DAT1 gene. Several studies report that commonly found polymorphisms in the DAT1 locus are associated with ADHD (Barr, Wigg, Bloom, Schachar, Tannock, Roberts, Malone, & Kennedy, 2000; Cook, Stein, Krasowski, Cox, Olkon, Kieffer, & Leventhal, 1995; Daly, Hawi, Fitzgerald, & Gill, 1999; Gill, Daly, Heron, Hawl, & Fitzgerald, 1997; Swanson et al., 2000; Waldman, Rowe, Abramowitz, Kozel, Mohr, Sherman, Cleveland, Sanders, Gard, & Stever, 1998). In a meta-analysis of 11 family-based studies, Cook (2000) found the association between the DAT1 gene and ADHD to be highly significant (p < .0001). It is important that levels of hyperactive–impulsive symptoms are correlated with the number of DAT1 high-risk alleles but levels of inattentive symptoms are not (Waldman et al., 1998). A role for polymorphisms of the DAT1 gene in ADHD is consistent with the centrality of the striatum in ADHD because DAT plays a particularly important role in the striatum. It is also consistent with the efficacy of methylphenidate in treating ADHD, because methylphenidate acts directly on DAT function (Dresel, Krause, LaFougere, Brinkbaumer, Kung, Hahn, & Tatsch, 2000; Seeman & Madras, 1998; Shenker, 1992; Volkow, Gur, Wang, Fowler, Moberg, Ding, Hitzemann, Smith, & Logan, 1998). Further, there is evidence that nicotine may act directly on DAT in a way similar to that of methylphenidate (Krause et al., 2003; Krause, Dresel, Krause, Kung, & Tatsch, 2000; Krause, Dresel, Krause, Kung, Tatsch, & Ackenheil, 2002). Indeed, DAT binding specifically in the striatum has been found to be related to motor hyperactivity but not to inattentive symptoms (Jucaite, Fernell, Halldin, Forssberg, & Farde, 2005).

If the striatum is potentially the primary site for neurobiological dysfunction in ADHD, what is the primary site for dysfunction in ADD? There has been far less research on ADD, especially excluding individuals misdiagnosed as having ADD rather than subthreshold combined-type ADHD. However, the neurobiological, cognitive, and behavioral profile of children with ADD strongly implicates a primary disturbance in prefrontal cortex. Whereas polymorphisms in the DAT1 gene are hypothesized to be more strongly linked to ADHD than ADD, the 7-repeat allele polymorphism of the DRD4 gene is more strongly linked to ADD then to ADHD (Rowe, Stever, Giedinghagen, Gard, Cleveland, Terris, Mohr, Sherman, Abramowitz, & Waldman, 1998). The dopamine receptor subtype, DRD4, is present in prefrontal cortex in humans, but not in the striatum (Meador–Woodruff, Damask, Wang, Haroutunian, Davis, & Watson, 1996). Hence, a link with the DRD4 gene implicates prefrontal, rather than striatal, involvement. In the human prefrontal cortex, mRNAs for the dopamine receptor subtypes (DRD1 and DRD4) are the most abundant, although the other dopamine receptor subtypes are present. In the human striatum, in contrast, receptors are abundant for, and limited to, D1, D2, and D3 (Meador–Woodruff et al., 1996). Similarly, in the rhesus monkey, DRD4 is densely localized to prefrontal cortex and the hippocampus, with significantly lower levels in the striatum (De La Garza & Madras, 2000). Although DRD4 and DRD5 expression is noticeably higher in the cortex than the striatum of the rhesus brain, levels of DRD1 and DRD2 mRNAs are noticeably higher in the striatum than in the cortex. Consistent with an association between DRD4 polymorphism and ADD is Auerbach, Benjamin, Faroy, Geller, and Ebstein's finding (2001) of a significant relation between individual differences in sustained attention and working memory on the one hand and polymorphism of the DRD4 gene on the other hand in normal infants (those with the 7-repeat allele performing worse). Also consistent with this is that DAT1 gene expression has been found to preferentially affect caudate volume, whereas DRD4 gene expression preferentially affects prefrontal gray matter volume (Durston et al., 2005). However, the finding that ADHD children with the DRD4 7-repeat allele required higher doses of methylphenidate is inconsistent with this (Hamarman, Fossella, Ulger, Brimacombe, & Dermody, 2004).

No brain region functions in isolation. The striatum has close links with prefrontal cortex and there is considerable evidence that a disturbance in frontal–striatal circuitry is found in ADHD (e.g., Casey et al., 1997; Castellanos, 1997; Hale, Hariri, & McCracken, 2000; Heilman, Voeller, & Nadeau, 1991). Brain regions participate in more than one circuit. The patterns of deficits often seen in ADD (such as problems with math calculation, language, and working memory, and lethargy (not due to depression) implicate a frontal–parietal circuit (e.g., Chochon, Cohen, van de Moortele, & Dehaene, 1999; Peers, Ludwig, Rorden, Cusack, Bonfiglioli, Bundesen, Driver, Antoun, & Duncan, 2005; Ravizza, Delgado, Chein, Becker, & Fiez, 2004; Rivera, Reiss, Eckert & Menon, 2005; Simon, Mangin, Cohen, Le Bihan, & Dehaene, 2002; van Honk, Schutter, Putman, de Haan, & d'Alfonso, 2003).

Motivational Component to ADD
Although the literature and diagnostic manuals refer to children with ADD as easily distracted, I would like to propose that a more accurate description is that they are easily bored. Their problem lies more in motivation than it does in inhibition. ***End Quote

~Bold, Underlining, and Color changes Mine~


Oh man there is my BA = bordum adversion -LOL

Instead of all this they simply could have listened to ADDers to begin with -

Okay frontal lobes not frontal lobe well sense the frontal lobes are not the end all and be all of who we are I would say they are trying to "get it" but must dig deeper. . . frontal lobes executive functions too simplistic of an explanation. . . . . but I guess I won't confuse every one at once here.

What we have here is people with ADD and ADHD are easily bored and hey there are different sub-types which may or may not have diddlie to do with the frontal lobes executive functions even though the way I function off medication is more indicative of having too many executives in the functioning. I take the orange pills so some of the executives in my mind will shut up so the working part of the brain can function. Any one who has experienced the situation of too many chief and not enough Indians should be able to relate to my analogy of executives and functioning which many don't they actually prevent functioning especially if there are too many of them in the real work life atmosphere


Thanks for reading I am off. . . . to where hmmm I make that up as I go along but must wiggle . . . .
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  #21  
Old 08-10-08, 12:43 AM
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Re: Dopamine + ADD // Norepropine + ADD

Quote:
Originally Posted by meadd823 View Post
Well the forntal lobe thing looks like it might be a flop = like we are surprized.


Performance of children with ADHD on tests sensitive to frontal lobe dysfunction.

The performances of 20 children with attention deficit hyperactivity disorder (ADHD) were compared with those of 20 matched normal controls on a battery of neuropsychological tests. The ADHD children exhibited impaired function in reading comprehension, verbal learning and memory, and on the Information, Arithmetic, Digit Span, Block Design, and Coding subtests of the Wechsler Intelligence Scale for Children-Revised, but they performed nearly normally on measures of verbal and design fluency and on the Wisconsin Card Sorting Test. The hypothesis that disturbances in frontal lobe function related to impulse control may be responsible for the cognitive impairments observed in ADHD was not supported. Inability to control and direct attention appears to be more central to the pathophysiology of this disorder.
***End Quote

{bold and underlining mine}

Can any one say no shhhhht sherlock?
I'm not sure what the implications of this are? Are you trying to refute the studies that prove ADHDers have less activity in the frontal lobe regions?
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Old 08-11-08, 01:39 AM
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Re: Dopamine + ADD // Norepropine + ADD

Quote:
I'm not sure what the implications of this are? Are you trying to refute the studies that prove ADHDers have less activity in the frontal lobe regions?
I am questioning interpretations of said study results

Are these decreases we see on imaging the cause of ADD or the result of it


To present as if this is known for sure is not fully truthful - If I remember right we are still working on the chicken and the egg question . . . .EF is a collection of processes whose interaction is poorly understood -
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Old 08-11-08, 01:51 AM
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Re: Dopamine + ADD // Norepropine + ADD

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Originally Posted by meadd823 View Post
I am questioning interpretations of said study results

Are these decreases we see on imaging the cause of ADD or the result of it


To present as if this is known for sure is not fully truthful - If I remember right we are still working on the chicken and the egg question . . . .EF is a collection of processes whose interaction is poorly understood -
I think I covered my specific contention with this in the PM reply I sent you.

I'm not sure what your position is. As a mod with so many posts, I'm sure you've run into some people who have indeed suffered great frustration/pain due to severe ADHD.
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Old 08-11-08, 03:29 AM
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Moderators are members here too . . . .

Quote:
I'm not sure what your position is. As a mod with so many posts, I'm sure you've run into some people who have indeed suffered great frustration/pain due to severe ADHD.
I am not posting as a moderator but as a member who happens to be a moderator - My status on staff doesn't make my personal opinion any more to less valuable that any other members We are a peer to peer support group - like the rest of you I share knowledge based upon my personal experience in dealing with ADD. My opinion and perspectives are just that my opinion and perspectives

===========================Moderator Notes=======================

My moderator status gives me authority to enforce the guidelines here at ADDF period.

All post written as a moderator will have green bold text and have moderator in the title -

All moderator posting will be dealing strictly with ADDF guidelines NOT matters of science, ADD treatments or opinion.
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