Posted by Jason911 on March 3, 2002, at 11:08:07
In reply to Wellbutrin increases or decreases dopamine?, posted by Jill K. on March 3, 2002, at 2:41:40
Listen. Wellbutrin only midly block the uptake of dopamine but DECREASES the amount of dopamine in your brain. This IS what happens and pdocs tend to deny this. It is a proven fact. What is does do is dramatically increase your NE (norepinephrine) levels quite markedly. The reason why you smoke so much well.... read this. I recommend Jumex (selegiline).
"A recent New York study showed that smokers had on average 40% less of the enzyme, monoamine oxidase type-B, in their brains than non-smokers. Levels returned to normal on their giving up smoking. Not merely is the extra dopamine in the synapses rewarding. The level of MAO-b inhibition smokers enjoy apparently contributes to their reduced incidence of Parkinson's and Alzheimer's disease. Unfortunately they are liable to die horribly and prematurely of other diseases first.
One option which the dopamine-craving nicotine addict might wish to explore is switching to the (relatively) selective MAO-b inhibitor selegiline, better known as l-deprenyl. Normally the brain's irreplaceable complement of 30-40 thousand odd dopaminergic cells tends to die off at around 13% per decade in adult life. Their death diminishes the quality and intensity of experience. It also saps what in more ontologically innocent times might have been called one's life-force.
Whatever the full explanation, deprenyl-driven MAOI-users, unlike cigarette smokers, are likely to be around to enjoy its distinctive benefits for a long time to come, possibly longer than their drug-na´ve contemporaries. For in low doses, deprenyl enhances life-expectancy, of rats at least, by 20% and more. It enhances drive, libido and motivation; sharpens cognitive performance both subjectively and on a range of objective tests; serves as a useful adjunct in the palliative treatment of Alzheimer's and Parkinson's disease; and makes you feel good too. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs. At dosages of below 10-15 mg daily, deprenyl retains its selectivity for the type-B MAO iso-enzyme. At MAO-B-selective dosages, deprenyl doesn't provoke the "cheese-effect"; tyramine is also broken down by MAO type-A. Deprenyl isn't addictive, which probably reflects its different delivery-mechanism and delayed reward compared to inhaled tobacco smoke. Whether the Government would welcome the billions of pounds of lost revenue and a swollen population of energetic non-taxpayers that a switch in people's MAOI habits might entail is unclear. " -Jason911
"..... Selegiline, also known as l-deprenyl, is an irreversible and (relatively) selective MAO-B inhibitor.
The enzyme monoamine oxidase has two main forms, type A and type B. They are coded by separate genes. MAO may be inhibited with agents that act reversibly or irreversibly; and selectively or unselectively. These categories are not absolute. MAO type-A preferentially deaminates serotonin and noradrenaline, and also non-selectively dopamine. Type B metabolises dopamine, phenylethylamine (the chocolate amphetamine) and various trace amines.
At dosages of below 10-15 mg daily, selegiline retains its selectivity for the type-B MAO iso-enzyme. In contrast to unselective and irreversible MAO inhibitors such as tranylcypromine (Parnate) and phenelzine (Nardil), both of which strongly potentiate the catecholamine-releasing effect of tyramine, selegiline inhibits it. This ensures that selegiline does not induce the hypertensive "cheese effect".
Selegiline has immune-system-boosting and anti-neurodegenerative effects. Its use increases the level of tyrosine hydroxylase, growth hormone, cerebral nitric oxide and the production of key interleukins. Selegiline offers protection against DNA damage and oxidative stress by hydroxyl and peroxyl radical trapping; and against excitotoxic damage from glutamate. In addition, selegiline stimulates the release of superoxide dismutase (SOD). SOD is a key enzyme which helps to quench damaging free-radicals.
Taken consistently in low doses, selegiline tends to extend the life-expectancy of rats by some 20%; enhances drive, libido and endurance; and independently improves cognitive performance in Alzheimer's patients and in some healthy normals. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs.
Selegiline also protects the brain's dopamine cells from oxidative stress. The brain has only about 30-40 thousand dopaminergic neurons in all. We tend to lose perhaps 13% a decade in adult life. An eventual 70%-80% loss leads to the dopamine-deficiency disorder Parkinson's disease, frequently foreshadowed by depression.
Selegiline retards the metabolism not just of dopamine but also of phenylethylamine, a trace amine also found in chocolate and released when we're in love.
At MAOI-B-selective dosages, selegiline is typically less effective as a mood-brightener than other dopaminergics such as amineptine. And by the refined standards of posterity, we are all probably glorified glue-sniffers: the impending Post-Darwinian Transition to paradise-engineering has dreadfully crude origins. But by today's standards, at least, selegiline is still a potentially valuable life-enriching agent...."
> My pdoc has also recommended wellbutrin for my social phobia/apathy. I am also on neurontin for mild anxiety. He thinks I need more dopamine. He says that is why I smoke cigarettes. I read wellbutrin actually decreases the dopamine and that is why it has a low incidence of inducing mania.
> Does anyone know whether wellbutrin helped with dopamine or not?