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A major function of the Dopamine Beta Hydroxylase (DBH) gene is to produce an enzyme of the same name, dopamine beta hydroxylase. This enzyme is responsible for converting the important nervous system chemical dopamine into another important chemical called norepinephrine. Individuals with ADHD often show abnormal levels of one or both of these chemicals (typically on the low side).
Probably low DHB make a poor production of brain noradrenaline, this one is important too for attention and vigilance; Too much is bad but too low is also very bad.
DHB need some copper and vit C to produce NE If ADD people with low DHB (genetic) take stimulant, do you think that the “high release” from stimulant deplete post-synaptic noradrenaline quickly ? and make this people worse (depression, anergia, fatigue) ?
Jean;4776 wrote:A major function of the Dopamine Beta Hydroxylase (DBH) gene is to produce an enzyme of the same name, dopamine beta hydroxylase. This enzyme is responsible for converting the important nervous system chemical dopamine into another important chemical called norepinephrine. Individuals with ADHD often show abnormal levels of one or both of these chemicals (typically on the low side).Probably low DHB make a poor production of brain noradrenaline, this one is important too for attention and vigilance; Too much is bad but too low is also very bad.
DHB need some copper and vit C to produce NE If ADD people with low DHB (genetic) take stimulant, do you think that the “high release” from stimulant deplete post-synaptic noradrenaline quickly ? and make this people worse (depression, anergia, fatigue) ?
Show me some references documenting this.
@DrMariano 4779 wrote:
Show me some references documenting this.
In fact, I’ve no reference it’s just speculative, I try to understand why some ADHD people have depressive symptoms or exhaustion with a low dose stimulant after fews day of treatment. May be the decrease presynaptic alpha 2 receptors that deplete catecholamine level. In fact, I think that are a equilibrum of synthesis:release and when the excess release is more important than the synthesis it’s is logic that you exhaust the system; Right or wrong ?
” the administration of d-amphetamine did not have any effect on alpha2-receptor binding in ADHD boys. Those who did not demonstrate improvement from d-amphetamine treatment had the lowest alpha2-receptor binding compared with both responders and controls. These findings suggest a normal alpha2-adrenergic activity in ADHD boys who respond to d-amphetamine, in contrast to a possible increase in NE release in ADHD boys who are amphetamine nonresponders, perhaps secondary to decreased alpha2-adrenergic receptors.[1,2]”
Zametkin AJ, Hamburger SD. The effect of methylphenidate on urinary catecholamine excretion in hyperactivity: a partial replication. Biol Psychiatry. 1988;23:350-356. Abstract
Zametkin AJ, Karoum F, Linnoila M, et al. Stimulants, urinary catecholamines, and indoleamines in hyperactivity. A comparison of methylphenidate and dextroamphetamine. Arch Gen Psychiatry. 1985;42:251-255.
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