great post! Thanks!
Would you still think this effective post-cycle for drugs that have no prolactin-type sides?
What about rebound effect coming off Deprenyl?
Very, very interesting post, BBB. The question I am drawing from this is: Based upon your observations up to now, how do you feel about Selegiline as an alternative to, say, cabergoline, during a cycle of tren or deca? I don’t know enough about the exact mechanisms of dopamine agonists/prolactin inhibitors, and whether there should be a distinction between the two or if the line is more blurred. Would you say that, based upon what you know at this point, Selegeline may be a viable alternative to cabergoline for prolactin inhibiting purposes, or that it would be better used at more of a “supplement” after the fact?
I have started this. It has a short half life, but its MAO-B inhibition half life is around 40 DAYS.
Prescribing guidelines are for Parkinson’s disease. Taking 5-10 mg/day would probably make most normal people feel dopamine overload - morning head aches, stuffy feeling and not unlike a mild hangover. Most would do well starting at 5-10mg per WEEK.
As far as dopamine effects go, it will be cumulative with caber, trazodone, Wellbutrin and other dopergenic AD meds [anti depressive]. If using more than one, you will have to cut back on something. May need to drop an AD med, and if it works out that way, you might feel better overall and can also then not have SSRI libido loss.
Some take PEA [phenylethylamine] which rapidly is degraded by MOA. With deprenyl, PEA is quite effective in low doses. High doses of PEA with deprenyl use can be uncomfortable. PEA does not need to be taken at the same time as deprenyl and may need to be taken more frequently.
I feel more alert and and more active.
With deprenyl+PEA I am finding a great boost of libido that caber alone did not provide for me. Orgasms are very very intense. I started both together and cannot report on deprenyl-PEA.
How things work over time remains to be seen as the body adapts to change and initial beneficial results can diminish. Probably not a good idea to take these things without a break.
Guys, are these considered research chems?
Very interesting stuff…
PEA is a supplement and available as a bulk powder as well as caps.
Deprenyl is a prescription drug.
Thanks. Figured as much.
Does anyone know if liquid selegiline (research chem) would be as effective as the tablet version (or would it have the suffer the same problems as liquid vs. tablet caber)?
also another supposed benefit of these Dopamine agonists, MAO-B inhibitors and the like which i have experimented with is their effects on leptin levels and therefor the benefits on fatloss while dieting.
Lyle Mcdonald has written a whole book on Bromocripine (a D1 agonist) and its use for this, definitely worth a read if your at all interested in the neurochemistry of body composition, but it may be a bit basic for guys like BBB and KSman
i myself tried pergolide (a D1 and D2 agonist) which is basically stronger than bromocriptine for a while dieting and it did work very well
in my experience it enabled a high rate of fatloss to be sustained for much longer, and at the same time being much more comfortable throughout the dieting period. energy was higher, i was able to have a bigger calorie deficit and do more cardio than i normallly would and still maintain muscle mass.
its like my body/brain was quite happy to burn off fat instead it being a constant battle to get my fat lower than its ever been.
in laymans terms it tricked my brain into thinking i was being well fed when really i was flogging myself
and lowers your bf ‘set point’ (only while on the drug though)
this is a summary of how bromocriptine works from the book
We know that low leptin (or leptin resistance) leads to changes in NPY and
CRH which negatively affects metabolism. We know that bromocriptine (or
bromocriptine plus another drug) activates the D2 (and D1) receptor and normalizes
levels of NPY and CRH (and thus metabolism). So we ask the logical question: does
leptin work by changing brain DA levels?
The answer, as you might have guessed (or I wouldnâ??t have written this book) is
yes. As it turns out, a group of neurons in the hypothalamus (the area of the brain
which plays a key role in controlling hunger) which produce DA in the brain have leptin
receptors (57). This suggests that binding of leptin to those neurons is affecting DA
levels.
Perhaps more conclusively, a recent study has measured both leptin and DA
levels in humans who were dieting. As leptin dropped in response to the diet, levels
of DA dropped as well (58) supporting the existence of a causal link between the two;
cortisol levels increased as well, which makes sense considering the effects of leptin
on CRH. As leptin drops, so do brain DA levels causing NPY/CRH levels to become
abnormal which screws up metabolism; as leptin goes up so do brain DA levels
(assuming no leptin resistance) causing NPY/CRH to normalize and fix metabolism.
That s the punch line: DA is the link between leptin and metabolism via
NPY/CRH. Bromocriptine mimics DA in the brain, making the brain think that all
systems are normal even if theyâ??re not.
Related to this, I want to mention fat cell apoptosis (death) again. It turns out
that injecting leptin into the brains of mice can cause fat cell apoptosis to occur (59).
And a recent abstract shows that bromocriptine administration has the same effect
(60), once again suggesting that both leptin and bromocriptine are working through
the same basic mechanisms. That mechanism is DA. This is all summed up in
graphic on page 68.
So normally leptin would bind to the brain, increasing DA levels. That DA would
activate D1 and D2 receptors, normalizing levels of NPY and CRH, which would lead
to increased metabolic rate, fat burning, testosterone, and thyroid, and decreased
cortisol and appetite. When leptin drops, DA levels drop, NPY and CRH go up, and
that signals the adaptations to dieting: decreased metabolic rate, crashing hormones,
increased hunger, etc, etc.
Since bromocriptine can bind to the D2 receptor, it partially mimics the effects
of leptin, correcting NPY and CRH and normalizing metabolism. Thatâ??s the punch
line, bromocriptine allows us to â??trickâ?? the brain into thinking all systems are normal
while avoiding the issues of low leptin or leptin resistance.
Although leptin is still the key regulator in â??tellingâ?? the brain whatâ??s going on,
there are other neurochemicals that leptin ultimately works through. Although there
are many already discovered and many more to be found, neuropeptide Y and
corticotropin-releasing hormone (NPY and CRH) appear to be two of the main ones.
In the various models used, from OB mice to humans, NPY and CRH show
characteristic changes in response so such things as dieting and starvation, causing
the body to adapt in all the (negative) ways weâ??ve talked about. Changes in NPY and
CRH affect metabolic rate, hormonal levels, appetite, fat burning, and calorie
partitioning. Normalizing levels of those neurochemicals normalizes the rest of the
metabolic picture.
It turns out that NPY and CRH are controlled a little further upstream by levels of
brain dopamine (DA). That is, normally leptin would bind to specific neurons, raising
brain DA, which would then control NPY and CRH levels. As leptin drops (dieting, OB
mouse) or when leptin resistance develops (obese humans, DIO rat), there is less
DA produced. This makes the brain â??thinkâ?? itâ??s starving and NPY and CRH change,
affecting everything else downstream negatively. Bromocriptine, by activating the DA
receptors directly, can â??trickâ?? the brain into thinking itâ??s not starving, so that the normal
metabolic adaptations donâ??t occur. And, finally, thatâ??s how bromocriptine works.
I believe extra dopamine should also increase GH release, though to what degree I’m not certain.
I posted this in the thread Bushy started in Supplements & Nutrition forum about restless leg syndrome and figured it should go in here as well.
One thing I read about selegeline is that it will cause a false positive test for amphetamines/methamphetamine (it shares metabolites with them). Something to think about for those who want to self medicate and could be required to take a drug test.
Can anyone can confirm if this is the case or not? I think if it is then it is something people should be aware of.
[quote]waldo21212 wrote:
I posted this in the thread Bushy started in Supplements & Nutrition forum about restless leg syndrome and figured it should go in here as well.
One thing I read about selegeline is that it will cause a false positive test for amphetamines/methamphetamine (it shares metabolites with them). Something to think about for those who want to self medicate and could be required to take a drug test.
Can anyone can confirm if this is the case or not? I think if it is then it is something people should be aware of.[/quote]
That is my understanding as well.
After reading this post I made a purchase. On it for 2 weeks @ 2.5 mg a day. I do feel a difference in alertness overall energy and have noticed positive sexual side effects. Now, the real question. I bought enough to keep me on for a year and a half straight.
1)should I cycle?
2)will I get dependant?
3)will my brain eventually burn out on the stuff and stop producing dopamine if I stop taking it?
Happy so far- but I don’t wanna be a year down the road and find out I did damage to myself.
thanks
If you got it for fun, you should cycle. If you got it because you had symptoms, you may want to stay on it.
Probably need to taper out.
You do no want to use more than necessary. You will learn how you are affected and that is worth more than any generalizations.
I will be incorporating this in my pct in february, I will let you all know the outcome
Not looking for a source but should this be available from internet anabolic sources or RC’s?