rx medication and trt

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clayboy_123

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been on trt for a few weeks and also take rx dexedrine for adhd. although dexedrine is seeming to work less and less and i am having to resort to caffeine for energy and focus. my question is, does coming off the dexedrine allow you to have an increased feeling of wellbeing that perhaps dexedrine is masking? also, i am assuming my muscle building ability would increase as well, since dexedrine is masking that too?
 
damage007

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been on trt for a few weeks and also take rx dexedrine for adhd. although dexedrine is seeming to work less and less and i am having to resort to caffeine for energy and focus. my question is, does coming off the dexedrine allow you to have an increased feeling of wellbeing that perhaps dexedrine is masking? also, i am assuming my muscle building ability would increase as well, since dexedrine is masking that too?
Amphetamine derivatives generally do work less over time - as their TAAR activity maintains , but the secondary mode of action becomes more transparent in the long-run. Amisulpride can help abolish the loss of sensitivity (due to it's serotonin 7 blocking property), but you'd have to go it with caber as well to stop the prolactin effects. 5-HT7 antagonists are being developed as solo-tools for depression - but they also attenuate the amphetamine inhibition of dopamine, indicating that eventually, amphetamines raise serotonin as tolerance develops, which leads to said inhibition and sensitivity alteration.
Effects of the serotonin 5-HT(7) receptor antagonist SB-269970 on the inhibition of dopamine neuronal firing induced by amphetamine. - PubMed - NCBI
Amphetamine Mechanisms and Actions at the Dopamine Terminal Revisited
A mechanism for the development of tolerance to amphetamine in rats - Springer
Psychopharmacology (Berl). 2009 Jul;205(1):119-28. doi: 10.1007/s00213-009-1521-8. Epub 2009 Apr 1.
Amisulpride is a potent 5-HT7 antagonist: relevance for antidepressant actions in vivo.
Abbas AI1, Hedlund PB, Huang XP, Tran TB, Meltzer HY, Roth BL.
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Abstract
RATIONALE:
Amisulpride is approved for clinical use in treating schizophrenia in a number of European countries and also for treating dysthymia, a mild form of depression, in Italy. Amisulpride has also been demonstrated to be an antidepressant for patients with major depression in many clinical trials. In part because of the selective D(2)/D(3) receptor antagonist properties of amisulpride, it has long been widely assumed that dopaminergic modulation is the proximal event responsible for mediating its antidepressant and antipsychotic properties.
OBJECTIVES:
The purpose of these studies was to determine if amisulpride's antidepressant actions are mediated by off-target interactions with other receptors.
MATERIALS AND METHODS:
We performed experiments that: (1) examined the pharmacological profile of amisulpride at a large number of central nervous system (CNS) molecular targets and, (2) after finding high potency antagonist affinity for human 5-HT(7a) serotonin receptors, characterized the actions of amisulpride as an antidepressant in wild-type and 5-HT(7) receptor knockout mice.
RESULTS:
We discovered that amisulpride was a potent competitive antagonist at 5-HT(7a) receptors and that interactions with no other molecular target investigated in this paper could explain its antidepressant actions in vivo. Significantly, and in contrast to their wild-type littermates, 5-HT(7) receptor knockout mice did not respond to amisulpride in two widely used rodent models of depression, the tail suspension test and the forced swim test.
CONCLUSIONS:
These results indicate that 5-HT(7a) receptor antagonism, and not D(2)/D(3) receptor antagonism, likely underlies the antidepressant actions of amisulpride.
PMID: 19337725 [PubMed - indexed for MEDLINE] PMCID: PMC2821721 Free PMC Article

Neuropsychopharmacology. 2011 May;36(6):1275-88. doi: 10.1038/npp.2011.13. Epub 2011 Feb 16.
Pharmacological blockade of 5-HT7 receptors as a putative fast acting antidepressant strategy.
Mnie-Filali O1, Faure C, Lambás-Señas L, El Mansari M, Belblidia H, Gondard E, Etiévant A, Scarna H, Didier A, Berod A, Blier P, Haddjeri N.
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Abstract
Current antidepressants still display unsatisfactory efficacy and a delayed onset of therapeutic action. Here we show that the pharmacological blockade of serotonin 7 (5-HT(7)) receptors produced a faster antidepressant-like response than the commonly prescribed antidepressant fluoxetine. In the rat, the selective 5-HT(7) receptor antagonist SB-269970 counteracted the anxiogenic-like effect of fluoxetine in the open field and exerted an antidepressant-like effect in the forced swim test. In vivo, 5-HT(7) receptors negatively regulate the firing activity of dorsal raphe 5-HT neurons and become desensitized after long-term administration of fluoxetine. In contrast with fluoxetine, a 1-week treatment with SB-269970 did not alter 5-HT firing activity but desensitized cell body 5-HT autoreceptors, enhanced the hippocampal cell proliferation, and counteracted the depressive-like behavior in olfactory bulbectomized rats. Finally, unlike fluoxetine, early-life administration of SB-269970, did not induce anxious/depressive-like behaviors in adulthood. Together, these findings indicate that the 5-HT(7) receptor antagonists may represent a new class of antidepressants with faster therapeutic action.
PMID: 21326194 [PubMed - indexed for MEDLINE] PMCID: PMC3079839 Free PMC Article
 
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Adderall can also cause stress to an already taxed adrenal glad which TRT is pushing harder.
 
damage007

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Adderall can also cause stress to an already taxed adrenal glad which TRT is pushing harder.
Adrenal issues tend to come with hardcore stim use, especially in that class of drugs. Xanthine derivatives are pretty safe though.
 
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So i guess the answer to my two questions would yes?
 
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Adrenal issues comes from stress which meds may be just a small piece of the puzzle. Evaluation of history of personal and medical as well as other symptoms are needed to know what factors may be applicable to finding the underlying pathology.
 
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So i guess the answer to my two questions would yes?
When you come off of it, your dopamine system will have to re-boot, so Yes your abilities and balance can come back..
I would advise you to do blood work on cortisol and such after you go off.
Rhodiola Rosea + Cordyceps will help to regain normal hormone balance and recover from amphetamine dependence and such.

Another wonderful compound to help regenerate dopamine functioning post-amphetamine, is 9-me-bc AKA 9-methyl-beta-carboline....it is specifically used to regenerate dopaminergic neuron function and synaptogenesis (formation of synapses and nerve growth).

IF for some reason you choose to stay on the amphetamine, you should look into 5-HT(7) antagonists or possibly Shilajit which can help maintain and protect neuron integrity.
 
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Is there anything that can help with daily brain fog?
 
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Rhodiolia is counter productive with people with pre disposition to anxiety disorders and would not be suggested. I had too many doctor's patient who were taking the stuff which almost ended them being put on Benzo. Psychiatrists are not taught interactions of gene expressions with certain herbs which can be very dangerous combination.
 
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Rhodiolia is counter productive with people with pre disposition to anxiety disorders and would not be suggested. I had too many doctor's patient who were taking the stuff which almost ended them being put on Benzo. Psychiatrists are not taught interactions of gene expressions with certain herbs which can be very dangerous combination.
Rhodiola has anti-stress effects, it's effects on norepinephrine are there but not enough to make it a risk for most* anxiety prone individuals.
Plus using it with cordyceps will balance out it's effects due to adenosine regulation...so the net effect is still anti-stress/anti-anxiety.
 
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Clinically I will have to disagree with you as I have cases referred from doctors which shows a different story. Anedoctal and real world are 2 separate things. When it comes to adrenal function, I have been exposed to worst scenarios. I rarely suggest rhodiola as have in the past because of these out comes. There are 2 mechanism. Low dosage stimulates and high concentration suppress function. The higher dosage is made by only one company and works great in hyper adrenal function especially at night time. Everything out there needs to be revisit and this is the biggest mistake doctors are making. We are genetically not the same as gene expression is happening at birth why autism is on the rise. I found one of the possible reason for this to occur. I have been researching on finding a way to slow the process down just not there yet.
 
damage007

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Clinically I will have to disagree with you as I have cases referred from doctors which shows a different story. Anedoctal and real world are 2 separate things. When it comes to adrenal function, I have been exposed to worst scenarios. I rarely suggest rhodiola as have in the past because of these out comes. There are 2 mechanism. Low dosage stimulates and high concentration suppress function. The higher dosage is made by only one company and works great in hyper adrenal function especially at night time. Everything out there needs to be revisit and this is the biggest mistake doctors are making. We are genetically not the same as gene expression is happening at birth why autism is on the rise. I found one of the possible reason for this to occur. I have been researching on finding a way to slow the process down just not there yet.
You mean genetic abnormalties are existing at birth, part of this is because of vaccines..and it also has to do with the mother's genetics, drug use , including over-the-counter drugs during pregnancy...drugs that are normally safe under other circumstances e.g odansetron become NOT safe and a risk during fetal development. It only takes a little bit to pass through and act as 10x that amount for a growing fetus.

Additionally, heavy metals are implicated in autism and so are hormone matters . There's some evidence that exposure to transdermal hormone gels may influence the early brain development and thus increase risk of such disorders.

We know what these substances do to human adults, but the story for fetal development is always going to be more complex - and ... there can be 'cross-wiring' from other factors as well. Even something as 'light' as cigarrette use can become a problem.

Rhodiola is a substance where of course, like any other herb, contains multiple phytochemicals with diverse pharmacological properties, it will always come down to where it was obtained/cultivated, how it is extracted, and what active ingredients are 'at the surface'.

Due to unique differences in delivery methods as well - of course there will be mixed anecdotal reports..and as far as 'real-world', well...where do real - world results come from? Unbiased anecdotes, double-blind placebo's ? You have to realize, it always comes back to some sort of report which often has cited some sort of anecdote.
 
The Matrix

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Gene expression is happening with in the fetus which shouldn't happen for several years. Vaccinations are provided to close together. The number given have increased significantly in the past 10-20 years. If I vaccinate my kids it will be on delayed schedule and the bare minimal needed.
 

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