dopamine

[hardasnails1973]

What medical interventions can be used to raise only dopamine levels with out affecting everything else. Acetyl carnitine shows in studies to increase dopamine levels. Would this be worth trying when dopamine levels are dangerously way below the lower end of the range.

[DrMariano2]

@hardasnails1973 1097 wrote:

What medical interventions can be used to raise only dopamine levels with out affecting everything else. Acetyl carnitine shows in studies to increase dopamine levels. Would this be worth trying when dopamine levels are dangerously way below the lower end of the range.

Interventions can affect function at one or more different levels:

• Structure
• Signaling
• Metabolism
• Psychological-Behavioral
• Social-Environmental

Acetyl carnitine works at the level of cellular metabolism. This intervention may then cause changes at the signaling level. These changes may affect multiple signals, not only dopamine.

Dopamine is a signal. A change to dopamine signaling affects, in a cascade, multiple other signals, which then affect cellular metabolism.

Any change at one level may potentially cause a cascade of changes at several levels. It is thus difficult to isolate one change.

The best one can do is to simply change the component desired. In the case of attempting to dopamine in isolation, this includes adding Levadopa – the precursor to dopamine itself, or some other dopamine agonist, of which there are many.

—

A difficulty in treatment is that often one also wants to isolate the location of the intervention. The brain compartment, for example, as opposed to the body compartment. Even more specific, for example, pre-frontal cortex versus whole brain signaling. This is an ideal that is difficult if not impossible to do. Thus, an intervention may cause side effects through systemic or generalized activity rather than localized activity.

[hardasnails1973]

@DrMariano 1098 wrote:

Interventions can affect function at one or more different levels:

• Structure
• Signaling
• Metabolism
• Psychological-Behavioral
• Social-Environmental

Acetyl carnitine works at the level of cellular metabolism. This intervention may then cause changes at the signaling level. These changes may affect multiple signals, not only dopamine.

Dopamine is a signal. A change to dopamine signaling affects, in a cascade, multiple other signals, which then affect cellular metabolism.

Any change at one level may potentially cause a cascade of changes at several levels. It is thus difficult to isolate one change.

The best one can do is to simply change the component desired. In the case of attempting to dopamine in isolation, this includes adding Levadopa – the precursor to dopamine itself, or some other dopamine agonist, of which there are many.

I was looking at potentially selegliine 2.5 mgs a day orally then have him monitor the response.

I know Dr shippen uses TD selegiline with all his clients hoping to get a sense of well being or libido increase, but all people i have talked to have no response. If a person has low dopamine levels then a clinical response would be more evident from the selegiline.
Every natural route has been tried (fava beans, tyrosine,ect) now there needs to be proper medical interventions. Every psychiatrist he has been to favors adderall, or ritalin. These tend to make him feel spacey and low motivations. I told him that he should take this information to his treat psychiatrist so that it may help guide him to proper therapy. I saw a study on how selegiline and DPLA was used to treat ADDHD with a high success rate. I have no intention of dabbling with people’s brain chemistry because it is out of field and legally i do not want to be responsible. I am just trying to gather information so he can present to his treating practioner.

[DrMariano2]

@hardasnails1973 1099 wrote:

I was looking at potentially selegliine 2.5 mgs a day orally then have him monitor the response.

I know Dr shippen uses TD selegiline with all his clients hoping to get a sense of well being or libido increase, but all people i have talked to have no response. If a person has low dopamine levels then a clinical response would be more evident from the selegiline.
Every natural route has been tried (fava beans, tyrosine,ect) now there needs to be proper medical interventions. Every psychiatrist he has been to favors adderall, or ritalin. These tend to make him feel spacey and low motivations. I told him that he should take this information to his treat psychiatrist so that it may help guide him to proper therapy. I saw a study on how selegiline and DPLA was used to treat ADDHD with a high success rate. I have no intention of dabbling with people’s brain chemistry because it is out of field and legally i do not want to be responsible. I am just trying to gather information so he can present to his treating practioner.

Selegiline is a monoamine oxidase inhibitor. This means it will cause an increase in serotonin, norepinephrine, and dopamine signaling by reducing degradation of the signal. However, the increase in signaling is not equal. MAO inhibitors increase serotonin more than dopamine and norepinephrine. Selegiline becamse useful in Parkinson’s disease because it significantly increased dopamine, notwithstanding also increasing serotonin more. The serotonin increase is a side effect when treating Parkinson’s disease. However, when treating other conditions, the serotonin increase becomes an important consideration. For example, when attempting to improve libido by increasing dopamine, the serotonin increase will suppress libido directly as well as impairing erectile function directly, in addition to its indirect effects of reducing norepinephrine and dopamine signaling.

Standard stimulants like Ritalin and Adderall increase both dopamine and norepinephrine. The increase in norepinephrine may pose a problem. It may contribute to HPA Axis disregulation with cortisol signaling loss. It may increase pro-inflammatory signaling, which would then reduce motivation along with the cortisol signaling loss. It may increase anxiety, which would turn down libido. Etc. They are best used in very low doses as needed, just like Viagra, at the time of sex to help avoid the negative effects, when used primarily for sexual dysfunction. Of course, after use, insomnia is a problem when taken at night since norepinephrine is the primary signal for wakefulness. Couple this with the surge of norepinephrine to trigger an orgasm, and you have a recipe for post-coital stress and anxiety rather than relaxation.

[Jean]

Do you have success to with Gerovital 3; procaïne in it is a moderate inhibitors of MAO a ?

[clloyd]

This is one of my explorations into one day solving this mystery. After starting TRT (test +hcg) over a year ago, my pych meds starting lowering in doses..but not completely. In an effort to prove that my long term use of SSRI’s and adderall on HPA and/or HPTA, besides wanting the physical byproducts of HRT, my mid took a priority. After about 1 year into HRT, I had tapered off Lexapro completely. I had Xanax when needed. I had dropped to 10mg Adderall XR from 20-30mg. And still had to pop an Ambien once in a while. I got a major client and led a company as a Chief Restructuring Office into and out of a Chapter 11 bankruptcy, HArdest thing I ever had to do. After about a month off Lexapro (with everything fine), I had a breakdown of overwhelming feelings that kept me up until 3am crying and wanting to punchs walls. I was depressed about being depressed. I got back on 10mg LExapro that night. It reminded me of what Bravermen said about Serotinin being responsible for keep your head together so to speak. It’s genetic in my familiy, so I may have to accept it. However, my recent 1 month experience into low doses of GHRP+GHRH has seemed to start to reverse these patterns. Less Xanax, still being conservative on Lexapro, and probably on 10mg of Adderall because of a mental addiction.

Dr. Mariano, have you done any work into the overall sense of well bring that seems to not go away with GHRP+GHRH. My only theory is a repair or restart of HPA or HPTA. I don’t have adrenal fatigue symptoms right now. This is the best I have ever felt. I can’t take GHRP too late because of the cortisol spike. In Summary: I too don’t won’t to give up adequate levels of dopamine because of SSRI’s. I am hoping that moderate exogenous testosterone use and adderall help with dopamine. But there is no doubt that sometimes the norepinephrine over powers it –> creating more anxiety, etc. What I call the Elvis protocal. Slegeline was interesting, but I am not taking it now that I am back on Lexepro. I also considered bromocriptine.

@DrMariano 1100 wrote:

Selegiline is a monoamine oxidase inhibitor. This means it will cause an increase in serotonin, norepinephrine, and dopamine signaling by reducing degradation of the signal. However, the increase in signaling is not equal. MAO inhibitors increase serotonin more than dopamine and norepinephrine. Selegiline becamse useful in Parkinson’s disease because it significantly increased dopamine, notwithstanding also increasing serotonin more. The serotonin increase is a side effect when treating Parkinson’s disease. However, when treating other conditions, the serotonin increase becomes an important consideration. For example, when attempting to improve libido by increasing dopamine, the serotonin increase will suppress libido directly as well as impairing erectile function directly, in addition to its indirect effects of reducing norepinephrine and dopamine signaling.

Standard stimulants like Ritalin and Adderall increase both dopamine and norepinephrine. The increase in norepinephrine may pose a problem. It may contribute to HPA Axis disregulation with cortisol signaling loss. It may increase pro-inflammatory signaling, which would then reduce motivation along with the cortisol signaling loss. It may increase anxiety, which would turn down libido. Etc. They are best used in very low doses as needed, just like Viagra, at the time of sex to help avoid the negative effects, when used primarily for sexual dysfunction. Of course, after use, insomnia is a problem when taken at night since norepinephrine is the primary signal for wakefulness. Couple this with the surge of norepinephrine to trigger an orgasm, and you have a recipe for post-coital stress and anxiety rather than relaxation.

[Author]

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