I’m thinking of giving Modafinil a try but i’m not sure where to get it in the UK, most places selling it tend to be based in the US.Does anyone have any tips on finding a good place and the rules on ordering from abroad such as possible import duty?
Cheers
So I tried vinpocentine, loved it.
However, problems arose once I added in aniracetam and DMAE. I got a MASSIVE headache, unbearable actually. I was using the recommended dosage of both. 600 mg aniracetam 2x a day. DMAE 600mg 1-2 times a day. Any suggestions on how to alleviate this problem?
[quote]Meeko wrote:
So I tried vinpocentine, loved it.
However, problems arose once I added in aniracetam and DMAE. I got a MASSIVE headache, unbearable actually. I was using the recommended dosage of both. 600 mg aniracetam 2x a day. DMAE 600mg 1-2 times a day. Any suggestions on how to alleviate this problem? [/quote]
Single out which of the 2 is giving you a headache - Ani or DMAE. My guess is it’s the aniracetam, but once you find which it is, try lower the dose.
Alternatively, add centrophenoxine, or another source of choline.
I’m in the middle of exams right now (that are all essays). To study, and for the actual exam, I have been taking Vyvanse (Lisdexamfetamine
) at 30mg, sometimes 40mg.
The pill works wonderfully for 3-4 hours, then the comedown is terrible.
Are there any “brain function boosters” that I can take during this “come down” phase to make it more bearable? I have read that Vitamin C works, because Vitamin C and Vyvanse compete for the same receptors. Would DMAE, vinpo, etc. have any effect?
I have been taking DMAE and 5htp, and they seem to help, though minimally.
[quote]Meeko wrote:
I got a MASSIVE headache, unbearable actually.[/quote]
Are you taking a choline source. With most -racetams you need a choline source otherwise you get those headaches.
I recently turned 18 and I have been taking nootropics since I was about 16. Starting out I took only piracetam and choline, but recently I seem to have “perfected” my regimen.
Before breakfast:
1g L-Phenylalanine (Potentiates Selegiline/L-deprenyl)
100mg B6 (Potentiates Phenylalanine)
1.2g Acetyl L-carnitine
2g Pramiracetam (Pramiracetam dissolves in water)
I stay focused throughout the day and also do not have trouble staying up and focusing if I have to. Selegiline also supposedly helps you deal with having less sleep (i.e. I feel the same with 4 hours as 8 hours). The reason I started this regimen was because I needed an edge as I dual enrolled with a community college when I was in 11th grade and I am involved with many competitive academic clubs at my school (math team, etc). A few of the supplements I take double as both nootropics and supplements that helps with working out (caffeine, alpha lipoic acid, etc.)
[quote]NuRhoPsi wrote:
The increase in stress and ultimately CRF/ glucocorticoid production negated any of the nootropic benefits and actually caused a worse performance than if I had taken nothing.
[/quote]
You should try and get some Acetyl L-carnitiine. It is a nootropic that also inhibits the production of coristol.
[quote]Reht wrote:
[quote]Meeko wrote:
I got a MASSIVE headache, unbearable actually.[/quote]
Are you taking a choline source. With most -racetams you need a choline source otherwise you get those headaches.
I recently turned 18 and I have been taking nootropics since I was about 16. Starting out I took only piracetam and choline, but recently I seem to have “perfected” my regimen.
Before breakfast:
1g L-Phenylalanine (Potentiates Selegiline/L-deprenyl)
100mg B6 (Potentiates Phenylalanine)
1.2g Acetyl L-carnitine
2g Pramiracetam (Pramiracetam dissolves in water)
I stay focused throughout the day and also do not have trouble staying up and focusing if I have to. Selegiline also supposedly helps you deal with having less sleep (i.e. I feel the same with 4 hours as 8 hours). The reason I started this regimen was because I needed an edge as I dual enrolled with a community college when I was in 11th grade and I am involved with many competitive academic clubs at my school (math team, etc). A few of the supplements I take double as both nootropics and supplements that helps with working out (caffeine, alpha lipoic acid, etc.)[/quote]
Everything I’ve read about selegiline is it’s for older people; i.e., as you age you need more and more. The dose you’re taking is only half what they give to alzheimer’s patients - wildly inappropriate for an 18 yr old. (I am 40 and take 5mg once per week.)
Also, you indicate you are using it as a replacement for sleep; that practice will absolutely kill your neurons long-term. If you are smart and like learning the science, check out “The Promise of Sleep” by Dement, MD PhD; it’s a tome.
There is a difference between judicious use and abuse w/ noops, as w/ most things.
Otherwise, great post (mean it).
those of you with experience taking modanifil, did you also notice a synergistic effect with caffeine? i tried it out for the first time yesterday with a few sips of Spark and felt very mentally active.
sadly i took it too late and had a hard time getting sleepy.
[quote]B rocK wrote:
those of you with experience taking modanifil, did you also notice a synergistic effect with caffeine? i tried it out for the first time yesterday with a few sips of Spark and felt very mentally active.
sadly i took it too late and had a hard time getting sleepy. [/quote]
yes, moda and caffeine are quite sinergistic and the best thing of all is that the effect lasts for quite a while, much longer than caffeine alone.
[quote]Barret wrote:
[quote]B rocK wrote:
those of you with experience taking modanifil, did you also notice a synergistic effect with caffeine? i tried it out for the first time yesterday with a few sips of Spark and felt very mentally active.
sadly i took it too late and had a hard time getting sleepy. [/quote]
yes, moda and caffeine are quite sinergistic and the best thing of all is that the effect lasts for quite a while, much longer than caffeine alone.[/quote]
Just as I suspected (strokes mustache)…excellent.
What effects would aniracetam have on one’s hormonal profile, indirect or direct?
Also, I currently train for about 2 hours in the morning (skill work for my sport and weight lifting,) and 1-2 hours at night (intense skill work.) It is almost a necessity to take 900mg alpha gpc both before and after the morning session, and 900mg before sleep.
With such a high intake of choline precursors already, will I have to up this when I start daily aniracetam dosage?
(hours later)
Now let’s talk about these head aches that come with Moda, any thoughts? lol
Not a fan.
[quote]Defekt wrote:
What effects would aniracetam have on one’s hormonal profile, indirect or direct?
[/quote]
Off the top of my head, I don’t think anything beneficial or deleterious.
Things which enhance acetylcholine release (or prevent breakdown) such as DHEA, A-GPC, Huperzine-A likely have a positive impact on one’s hormonal profile.
We do know that enhancement of the acetylcholine levels in the brain has a direct, blunting affect on somatostatin, which through feedback loops will boost the release of GHRH, which in turn leads to higher GH levels.
Through some very complex and indirect feedback action on the endocrine system, I also suspect blunting somatostatin levels to youthful levels will enhance overall release of androgenic hormones, such as DHEA, Testosterone, Androstenedione, etc.
How?
I think rising somatostatin levels are likely problematic for many. It is important to note that somatostatin not only blunts GHRH → GH production, but also blunts some of the glycoproteins as well.
Hormones that are glycoproteins include:
Follicle-stimulating hormone
Luteinizing hormone
Thyroid-stimulating hormone
Human chorionic gonadotropin
Alpha-fetoprotein
Erythropoietin (EPO)
What does this mean? Well this is just a hypothesis/theory, but, that as we age, rising somatostatin levels not only blunt GH levels, but also blunt glycoprotein transport.
The Smooth Endoplasmic Reticula transports these glycoproteins, some inherently important to overall hormone signaling.
J Clin Endocrinol Metab. 1992 Jan;74(1):217-22.
Effects of dopamine and somatostatin on pulsatile pituitary glycoprotein secretion.
Samuels MH, Henry P, Ridgway EC.
Source
Division of Endocrinology, University of Texas Health Sciences Center, San Antonio 78284-7877
The hypothalamic factors dopamine (DA) and somatostatin (SRIH) inhibit pituitary glycoprotein secretion, but little is known regarding the effects of these factors on glycoprotein pulses. To address this question, 12 healthy volunteers underwent frequent blood sampling over 12 h at baseline and during 12-h infusions of DA and/or SRIH. TSH, LH, FSH, and alpha-subunit (alpha) levels were measured in all samples, and hormone pulses were located by Cluster analysis.
Both DA and SRIH suppressed TSH pulse amplitude by 70%, while SRIH decreased TSH pulse frequency as well.
Both infusions decreased LH pulse amplitude by 30-35%, but had no effect on pulse frequency. In contrast, neither infusion significantly altered FSH pulse parameters, although mean FSH levels declined 15%.
DA had no effect on pulsatile alpha secretion, while SRIH decreased alpha pulse frequency. Serum thyroid hormone levels declined during both infusions, but there were no major changes in serum sex steroid levels. *Wise Guy note: It would likely take years of elevated SRIH to inhibit levels of sex steroids. If they continued study indefinitely, this would have IMO likely happened.
Thus, the hypothalamic inhibitory factors DA and SRIH had divergent effects on glycoprotein hormone pulses. The major effects on pulse amplitude, rather than frequency, imply that these factors do not play major roles in the generation of glycoprotein pulses, although SRIH may directly affect the TSH and alpha pulse generators.
More Wise Guy Thoughts
Thus, we are seeing that rising Somatostatin levels may blunt pulsation of the glycoprotein transport system. This includes pulsation of LH and FSH as well as TSH.
Thus, we are seeing theoretically that rising Somatostatin levels may be part of a cascade of events that renders the SER faulty, and thus precursor hormone → hormone process faulty.
In effect, one would also be looking to blunt somatostatin levels via using a drug to do so. The one that is available that comes to mind is GHRP-6.
It is important to note that using GHRP-6 to blunt somatostatin levels is more important than using GHRP-6 to boost GH levels in itself. By blunting somatostatin levels, theoretically we are improving the pulsation of the glycoprotein transport system.
This could theoretically be why many who use GHRP-6 for extended periods of time (years) see many ancillary benefits beyond simple IGF-1 serum numbers (or no improvements in serum IGF-1 levels, yet experience improvements in symptoms related to aging, such as increased recovery time, increased slow wave sleep, increased mood and well-being, etc.).
This could theoretically be from improved pulsation of the glycoprotein transport system.
^whoa, that’s some education you got there
That was an awesome response. When I have some free time later today I will reread that, research the terms I don’t understand, and come back with a response. Thanks!
Okay. That was pretty informative and I understand most of it.
I get that increased somatostatin levels cause a wide array of lowered hormone levels through lowering either the frequency or intensity of glycoprotein transportation pulses (is this correct?) many of these exact processes are a little bit above my current level of understanding.
What I can’t understand from what you posted is whether or not increased dopamine decreased levels of hormones through a similar mechanism. I ask because I am wondering about the effects of l-tyrosine on these processes. This seems counter intuitive because I was under the impression that l-tyrosine increased the production of Thyroid-stimulating hormone, which is a glycoprotein.
[quote]Defekt wrote:
What I can’t understand from what you posted is whether or not increased dopamine decreased levels of hormones through a similar mechanism.
[/quote]
No, and if anything, the opposite. Dopamine has, at worst case scenario, no effect on androgenic hormone levels. There are some anecdotal reports of dopamine increasing testosterone levels, do to feedback mechanisms on other neurotransmitters and hormones which, at above baseline levels, suppress the HTPA. A couple that come to mind are serotonin and prolactin.
Dopamine boosting agents also represent a new wave of drugs used to treat ED.
Check this out.
http://resources.metapress.com/pdf-preview.axd?code=ukaljwyyr5ejcdrh&size=largest