Just because it doesn’t hit dopamine doesn’t mean it won’t make you feel good. An NRI will do that. In the USA we will never have a dopamine drug. The FDA won’t allow it which is insane. They even forced a European med off the market, made by the French pharmaceutical company Servier, that was excellent for dopamine. They didn’t want people here mail ordering it. The FDA would rather people suffer.
VTBalla34, We I’m happy atleast wellbutrin worked for you. I’m on 300mg a day right now and I don’t feel a thing. The only thing I notice is I get headaches in the evening. I’ve been on it for about 4 weeks at that level, so I have decided just to forget about it and I’m going to start tappering off it.
Brentf13, thats pretty interesting that the FDA blocks dopamine elevating drugs, I’m going to be leaving for Germany soon (for a year or maybe less). Maybe I should try to get that drug made by that French company. Do you know what it is called?
Danny880, thanks I’m going to go with a pregnenolone based supplement. Its not a cream but what do you think of :
Reset A.D. ---- I have heard alot of good things about it.
60 Capsules
Supplement Facts
Serving Size1Capsule
Servings Per Container60
Amount Per Serving % DV
Pantothenic Acid (As D-Calcium Pantothenate) 400mg 4,000%
Reset Complex 150mg â?
Rhodiola Rosea Root Extract 3% Rosavins, Schizandra Berry, Licorice Root
Adrenal Relief Complex 150mg â?
Bovine Adrenal Tissue, Pregnenolone
â?¡ Percent Daily Values are based on a 2,000 calorie diet
â? Daily Value not established
Other Ingredients:
Capsule Shell (Gelatin, Titanium Dioxide, FD&C Yellow #5), Magnesium Stearate, Microcrystalline Cellulose, And Silica.
If anyone else has taken it, I would love additional input on it.
jrvswim
you might want to consider not tapering off and give the meds time to do it’s job, though in my case at 300mg
was stimulating to the point i couldn’t sleep and was given low dose seroquel 37 mg for sleep and the wellbutrin very well save my life and decied a few yrs ago to go and been doing well with out, and if iwas depressed again that badly i would go on it.
I dont think its clear cut that one thing s is a NRI and another effects dopamine, theres a big cross over as stimilating one has an effect on the other. Wellbutrin is a NRI which then has a carry over effect onto dopamine release, its not going to be a strong as supplementing directly with dopamine but there is some effect there for sure. most stimulants effect both neurotransmitters too.
jrvswim, keep us updated on how u go with the pregnenolone.
cheers!!!
THanks for the input so far, I;ll be starting the pregnenolone but I’m honestly a bit afraid to do so. I know its pretty safe? Right? But, of course on the web I have found the occasonal horror story.
I feel like I just have some much to learn…so a more specific pregnenolone related question. Does taking pregnenolone supplements effect natural production? I think i have been reading that it does not, and really has very few negative side effects but I find it confussing in general since alot of the questions relate to people who are currently on trt (and i’m not sure if that complicates things).
I havent heard of any negative feedback type thing going on with pregnenolone if thats what your getting at?
Brentf13:
I know that you are speaking from personal experience here, and no one can argue with that, but I have to correct you on a few points. I am a doctor of pharmacy and specialize in clinical neurology and can assure you that dopaminergic drugs are used routinely and that bupropion is amongst them. Without getting into a pedantic amount of detail to illustrate the point let me try to clarify what I believe to be the confusion. To say that there is one dopaminergic pathway in the brain that is either modulated or not by a dopaminergic drug is patently false. There are many, many areas of the brain with various subsets and populations of dopamine receptors and different drugs affect select areas. Amphetimines (Adderal, Ritalin) modulate cortical dopaminergic receptors while parkinson’s medications (Levodopa, Requip, etc.) activate dopamine receptors in the nigrostriatal region (and other’s). Wellbutrin does not stimulate dopamine tracts in the limbic/mesocortical region directly which is why you don’t believe it has dopamine agonizing effects. Cocaine, methamphetime, and a few other street drugs do hit this area which is responsible for the pleasure/reward perceptions that are the hallmark of those drugs of abuse.
I just felt it necessary to clear that up.
1 Like
Tyson, do you have an opinion on the pregnenolone mentioned above?
And I’m really pulling at straws here, but I find this incredibly weird. I almost never wake up with morning erections. I don’t drink often but when I do, if I get reasonably drunk, I always wake up with wood. Which just does not make sense to me. I know alcohol raises estrogens and my estradiol is not that high…maybe I need it ?
Tyson what I was talking about is a straight up SDRI. There will never be one marketed as an antidepressant. The closest thing we have is Ritalin which is weak. There used to be an excellent one out of Europe called Amineptine. The FDA forced the manufacturer to remove it from the market for fear of mail order abuse here.
I’m aware of all of the Dopamine agonists and frankly I been on all of them. The only one worth a crap for mood and libido is Dosinex, which hits dopamine D2 receptors hard, and it poops out in the span of two weeks. In fact almost everything poops out from the body adjusting receptor sensitivity.
jrvswim,
The pregnenolone will only help if you have a specific condition i.e. adrenal insufficiency. If you don’t then it will not help but could potentially hurt given that it could be converted to the downstream products of pregnenolone e.g. cortisone, aldosterone, DHEA/S. Therefore, without lab confirmation that you are in fact adrenal insufficient (much less common than many here seem to think it is), I would tell you to hold off. Secondarily, I would not recommend the specific product you described above as it contains “adrenal extract” which is an animal byproduct that has been associated with some concern of prion disease transmission. Further it has negative evidence demonstrating lack of efficacy. Natural products are a crap shoot and the DHEA/hormone products have been shown in study to rarely (if ever) meet label claims and may actually be contaminated.
brentf13,
I assume you mean Dostinex (cabergoline). There aren’t many people who can tolerate that bad boy for long, it’s an ergot alkaloid and, as such, is a very dirty drug. 5-HT2B receptors, preferential distribution to the anterior pituitary causing D2 mediated prolactin release, etc. But that illustrates my point, while it is a D2 receptor agonist, so is ropinerole (anti-parkinsonian drug). What’s the difference then if they both act on the same receptor in the brain? Why can’t you use cabergoline to treat parkinson’s? Why doesn’t cabergoline dramatically antagonize D2 receptor blockers used to treat schizophrenia? If you only look at the receptor/neurotransmitter then you are only getting a partial picture. You have to know the region of the brain that the drug is distributed to primarily. Furthermore, the receptor subtypes are sub divided further than simply D1, D2, etc. The heterogeniety in these subtypes likely accounts for the action (and lack of action) of dopaminergic drugs at specific sites and therefore why drugs that propose to have the same mechanism of action do not produce similar effects in clinical practice.
Let’s use a quick (simplified) example to help illustrate this. Parkinson’s disease (PD) is a disease (at least primarily) due to loss of dopaminergic tone in the nigrostriatal pathway (and other’s) which controls voluntary movement. We treat it by stimulating dopaminergic neurons with either, direct agonists, or by giving dopamine directly in the form of L-dopa. If it were the case that all dopaminergic agonists (amphetimines/ritalin, cabergoline, etc.) or drugs that interfere with dopamine uptake (SDRI’s, wellbutrin) worked in the same manner, then the symptoms of PD would be ameliorated with any of them. This is not the case. They have no effect.
You are right though that often, increasing doses are required as the receptors downregulate due to overstimulation. It is interesting that this doesn’t happen in all of the disease states associated with deficiencies of dopamine.
Actually Dostinex is used for Parkinsons at a dose above 2mg a day and it was very effective. That dose caused heart valve problems so it’s no longer approved for Parkinsons. Now it’s used to treat high prolactin.
Amphetimines/ritalin dopamine agonists??? Amphetimine causes the release of dopamine and ritalin is a dopamine reuptake inhibitor. I wouldn’t expect those to work for Parkinsons because you can not release or block the reuptake of what is not there.
Brent,
I should have been more precise in that last post. I was post call and a little foggy. So let me clear that up. Amphetamines/ritalin are not technically dopamine agonists, true, they are treated as such because they stimulate zymogen granule release of endogenous dopamine (and NE) and therefore stimulate the D receptor. And ritalin (as well as amphetamines) will inhibit the reuptake of D and NE at escalating doses but this is not their primary mechanism of action.
So you’re right, in other words. Now as far as their potential use in PD you would be right if we are talking about late stage PD when there has been such a loss of dopaminergic neuronal mass that there wouldn’t be enough stored D to achieve a response. However, early on you would expect that there would be a significant effect in symptom reduction with amphetamine administration. I assure you this is not the case in clinical practice, at least not in tolerable dosages.
And this brings me to the next point about cabergoline. You are correct that it was used to treat PD in days past, so I should not have lumped it into the statement I made in the last post. But, what I was referring to was that in acceptable dosages it has little to no effect due to selective localization. You can overcome any specificity of a drug with increasing dosages.
This precludes absolute statements like the one I made above so I stand corrected. But just understand that the point I was trying to make is that at tolerable physiological dosages specificity becomes very important and cabergoline does not impart significant PD ameliorating effects at those doses.
I would love further inpt on trying pregnenolone and why the only mornings I wake with an erection, are nights after I drank alcohol.
Want to know about dopamine and Wellbutrin?
Brentf13: You need to explain yourself. In the context of the above, you look dumb and have some swallowing what you said.
If DHEA is low, that can reduce downstream hormones. Restoring to youthful levels can have great effects in some cases. Runaway conversion of DHEA–>E2 is rare and might be uncovering a possible liver estrogen clearance issue if that does occur. Statements that imply that taking DHEA always creates estrogen problems is simply false and misleading.
There isn’t any feedback mechanism for pregnenolone. Taking it will not affect ones own production.
Thanks KSman, I really appreciate your feedback. If i was going to choose dhea or pregnenolone, is there one you would pick over the other? Regarding the one you would pick, what dose would you recommend starting out?
Also based on my first page labs…could my E2 actually be too low?
Oral absorption of DHEA or pregnenolone varies vastly from one person to another. I absorb poorly and my brother absorbs well. So it is really not right imply that a starting dose is doing to be right. Many guys take 50mg DHEA. Pregnenolone is used much less often. Some are taking 50 or 100mg. Some get these as a compounded cream, can be both together. But the absorption is still a crap shoot. If there are thyroid problems, absorption might be low. DHEA is widely available. Pregnenolone will be found in better vitamin shops or the WWW. Both absorb as orals better with a fatty meal. Do not take these or, oil based supplements with oat meal or other high fiber foods.
[quote]KSman wrote:
Oral absorption of DHEA or pregnenolone varies vastly from one person to another. I absorb poorly and my brother absorbs well. So it is really not right imply that a starting dose is doing to be right. Many guys take 50mg DHEA. Pregnenolone is used much less often. Some are taking 50 or 100mg. Some get these as a compounded cream, can be both together. But the absorption is still a crap shoot. If there are thyroid problems, absorption might be low. DHEA is widely available. Pregnenolone will be found in better vitamin shops or the WWW. Both absorb as orals better with a fatty meal. Do not take these or, oil based supplements with oat meal or other high fiber foods.[/quote]
What is considered “low” DHEA?
KSman I know what Wiki and the drug manufacturer advertises. Independent studies have shown Wellbutrin to have no effect on Dopamine. Cruise on over the Dr Bob’s website and search for yourself. After using the drug common sense also shows the same. Wellbutrin weakly blocks the reuptake of dopamine and more strongly blunts it’s release. If the drug worked as advertised it would have a similar action and response rate to Ritalin which it does not.