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  • AADD Moderators: swilow | Vagabond696

Selegiline (l-deprenyl) - too good to be true?

I like the idea of cognitive enhancement + life extension too... but if I cant take pills and have them feel decent for even a month after, then its seriously hindering my temptation to do it.
 
^^mm me too. probably a bit less than you tho...
..i know this is very reductive...but my excitement at the prospect of living longer is limited by the prospect of a restricted lifestyle...
 
No point living forever if you can't enjoy your life. Why do you want to extend your life? Just enjoy what you have and then die and let the plants eat your body.
 
The prospect of never having a decent roll again... for the rest of your life... fuck, scary thought! Believe me I agree. The couple of occasions Ive rolled with Selegiline have not been diminished anyway
 
^^ damn *jealous* :p :)


the whole alcohol thing is a bit of a bummer too... even after one drink im getting sleepy...by two im ready to go to bed...even with stimulants..
 
Thought this was the best place to put my questions :)

Any ideas as to selegiline's method of action as a nootropic? Do you (you = anyone with good neuro knowledge) think that its due to the MAO-B inhibition, its catecholamine activity enhancement via increases in PEA and its metabolism to l-methamphetamine, or its propargylamine nature?

I realise its a combination of these, but where do you think the primary effect stems from?

Propargylamines have recently been thought to offer significant antioxidant activity what I remember, and so it could reduce the energy fraction that a neuron spends on repairing itself from oxidative stress.

On the other hand, the MAO-B inhibition may offer protection from ingested neurotoxins.

In theory it should be possible to distinguish between them based on how quickly the nootropic effect recedes after administration -- a quick return to normal would imply some sort of direct antioxidant nature, whereas a gradual decline would seem to reflect the gradual replenishment of MAO-B in the body.
 
All evidence points to MAO-B as selegiline has a high affinity as a substrate. Other oxidative stress mechanisms are undoubtedly affected such as NO induced apoptosis.

Here are some references you may like o chase up. Time's a bit restrictive ATM for me, but if there's anything you can't find and looks interesting, PM me and I'll attempt to locate it for you.

NOTE: My rushed in "cut and pasting" may have snipped some info. Yell if something which should be there isn't.

Institution
Boston Road Animal Hospital, 1235 Boston Road, Springfield, MA 01119, USA.
Editor
Kintzer, P. P.
Title
Adrenal disorders.
Source
Veterinary Clinics of North America, Small Animal Practice. 1997. 27: 2, i-xi, 173-425. many ref.
Abstract
The 14 reviews in this issue are entitled: Adrenal physiology; Glucocorticoid therapy: pharmacology, indications and complications; Diagnosis of canine hyperadrenocorticism; Imaging of adrenal gland disorders; Medical treatment of pituitary-dependent hyperadrenocorticism: mitotane; Management of canine pituitary-dependent hyperadrenocorticism with l-deprenyl (Anipryl); Pituitary corticotroph macrotumours: diagnosis and treatment; Diagnosis and management of canine cortisol-secreting adrenal tumours; Complications and concurrent disease associated with canine hyperadrenocorticism; Adrenal disorders in cats; Primary and secondary canine hypoadrenocorticism; Pheochromocytoma in dogs and cats; Adrenal incidentalomas: diagnostic workup of the incidentally discovered adrenal mass; and Adrenal gland disease in ferrets. There is an index.

ISSN
0195-5616
Update Code
199700
Year of Publication
1997
````````````````````````````````````````````


Institution
Box 673, Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642, USA.
Corporate Author
Parkinson Study Group.
Title
Effects of tocopherol and deprenyl on the progression of disability in early Parkinson's disease.
Source
New England Journal of Medicine. 1993. 328: 3, 176-183. 34 ref.
Abstract
In 1987 800 patients participated in a clinical trial examining the effectiveness of deprenyl (a monoamine oxidase inhibitor) and tocopherol (a component of vitamin E that traps free radicals) in the treatment of early Parkinson's disease. They were assigned to 1 of 4 treatments: placebo, active tocopherol and deprenyl placebo, active deprenyl and tocopherol placebo or both active drugs. The primary end point was the onset of disability prompting the administration of levodopa. After a mean ( plus or minus SD) follow-up of 14 plus or minus 6 months, there was no beneficial effect of tocopherol or any interaction between tocopherol and deprenyl. The beneficial effects of deprenyl, which occurred largely during the first 12 months remained strong and significantly delayed the onset of disability requiring levodopa therapy (hazard ratio, 0.50; 95% CI, 0.41 to 0.62; P less than 0.001). The difference in the estimated median time to the end point was about 9 months. The ratings for Parkinson's disease improved during the first 3 months of deprenyl treatment; the motor performance of deprenyl-treated patients worsened after the treatments were withdrawn. Deprenyl 10 mg but not tocopherol 2000 IU daily delayed the onset of disability associated with early, otherwise untreated Parkinson's disease.


Language
English.
Publication Type
Journal article.
ISSN
0028-4793
Update Code
199400
Year of Publication
1993
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Author
Glover, V. Pycock, C. J. Sandler, M.
Institution
Bernhard Baron Memorial Res. Lab., Queen Charlotte's Hospital, London, UK.
Title
Tyramine and depressive illness. The mechanism of the 'cheese effect' and its possible prevention by (-)-deprenyl.
Source
Psychopharmacology Bulletin. 1983. 19: 3, 496-500. 12 ref.
Abstract
The 'cheese effect', a dangerous hypertensive crisis that can occur when patients taking monoamine oxidase (MAO) inhibitors eat certain foods, particularly cheese, was investigated. The involvement of tyramine in this effect was studied using the MAO inhibitors clorgyline (selective for MAO-A) and (-)-deprenyl (selective for MAO-B), the former being particularly associated with hypersensitivity to oral tyramine. 1 micro M (-)-deprenyl in vitro blocked the potentiation of the tyramine-induced release of nor-adrenaline from rat brain slices by clorgyline. The possibility of using a combination of drugs to inhibit MAO-A without producing a 'cheese effect' is discussed.
CAS Registry Numbers
51-67-2

Language
English.
Publication Type
Journal article.
Update Code
198500
Year of Publication
1983
```````````````````````````````````````````````````````````````
Copyright Thomson 2004.
Author/Editor/Inventor
Riederer, Peter [Author]; Danielczyk, Walter [Author]; Gruenblatt, Edna [Author, Reprint Author; E-mail: [email protected]].
Institution
Neurochemical Laboratory, Clinic for Psychiatry and Psychotherapy, Bayerische Julius-Maximilians-Universitaet Wuerzburg, Fuechsleinstr. 15, 97080, Wuerzburg, Germany.
Country
Germany
Title
Monoamine oxidase-B inhibition in Alzheimer's disease.
Source
Neurotoxicology (Amsterdam). 25(1-2). January 2004. 271-277.
Publication Type
Article.
Literature Type
Literature Review.
ISSN
0161-813X

Language
English
Abstract
Alzheimer's disease (AD) is the most common cause of dementia in late life. There is still no clear-cut consensus whether this disease involves genetic or environmental factors or both. There is a great need to find a way to delay the disease, as delaying the onset of the disease will bring a great relieve on social and medical resources. The monoamine oxidase-B (MAO-B) inhibitors were shown to be effective in treating Parkinson's disease and possibly AD, with concomitant extension of life span. This article gives a short review on MAO-B inhibitors and their mechanism for neuroprotective effects in AD.


Year of Publication
2004

`````````````````````````````````````````````

Author/Editor/Inventor
Hobbenaghi, Rahim [Author]; Tiraihi, Taki [Author, Reprint Author; E-mail: [email protected]].
Institution
Departments of Anatomical Sciences and Pathology, School of Medical Sciences, Tarbiat Modarres University, P.O. Box 14155-4838, Tehran, Iran.
Title
Neuroprotective effect of deprenyl in sensory neurons of axotomized dorsal root ganglion.
Source
Clinical Neuropharmacology. 26(5). September-October 2003. 263-269.
Abstract
Spinal motoneuron neuroprotection by deprenyl was previously reported; the present study was carried out to evaluate neuroprotectivity in the dorsal root ganglion sensory neuron. The total neuron counts were calculated, and the axotomized sensory neurons of the dorsal root ganglion were significantly lower than those of the unaxotomized sides. Three secondary and three tertiary parameters were used. The secondary parameters were: the percentages of sensory neuron increase at the axotomized side (PNIA) and at the unaxotomized side (PNIU), and the percentage of neuronal response (PNR). The tertiary parameters were: the percentages of maximal response at the axotomized side (PMRA) and at the unaxotomized side (PMRU), and the percentage of maximal relative response (PMRR). Nonlinear statistical analysis using Gaussian, quadratic and logistic models of the tertiary parameters suggested that the data were bell-shape, which indicated that the data were biphasic. The data were divided into ascending and descending sets, and linear regression. They were analyzed according to Bent-hyperbola model and the ascending set was considered as a neurotrophic phase, while the descending one as a neurotoxic phase. The slops of PMRA were higher than that of PMRU, which indicates that the axotomized neurons were more sensitive than the unaxotomized neurons to the protective and neurotoxic effect of deprenyl. Moreover, the results showed that deprenyl had a proliferative effect on the dorsal root ganglion sensory neuron.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Author/Editor/Inventor
Kochman, Agata [Author, Reprint Author; E-mail: [email protected]]; Skolimowski, Janusz [Author]; Gebicka, Lidia [Author]; Metodiewa, Diana [Author].
Institution
Department of Pathological Anatomy, Medical University of Wroclaw, Marcinkowskiego 1, PL 50-368, Wroclaw, Poland.
Title
Antioxidant properties of newly synthesized N-propargylamine derivatives of nitroxyl: A comparison with deprenyl.
Source
Polish Journal of Pharmacology. 55(3). May-June 2003. 389-400.
Abstract
In our search for novel, low-toxic, cell-penetrable and neuroprotective antioxidants, we have designed a number of novel N-propargylamine derivatives of nitroxyl, named "JSAKs". The reactivity and antioxidative potency of two selected JSAKs and their parent nitroxyl against reactive oxygen species (ROS) were examined in vitro, in a cell-free gamma-radiolysis and in model Fenton-type reaction systems and compared with those of deprenyl, the investigated member of adjunct therapies in clinical neurology. The efficiency of JSAKs to suppress the oxidative degradation of a model target (deoxyribose), deprenyl and dopamine, caused by hydroxyl radical (.OH) was also investigated. The data demonstrated that the novel compounds, JSAKs, can act as promising antioxidants and protectors of targets against ROS toxicity, thus, providing a sound chemical basis for further comparative investigations of their activity in vivo. The findings were discussed from a mechanistic point of view as well as in terms of the structure-dependent, comprehensive properties of JSAKs as dual-function compounds: antioxidants and anti-apoptotic propargylamines. The novel class of N-propargylamine nitroxyls, JSAKs, may have potential implications for the experimental therapies of Parkinson's disease, where ROS mediate deleterious effects, because these compounds have an ability to either block or reduce the progression of neurotoxic cascade of brain damage.
``````````````````````````````````````````
Author/Editor/Inventor
Tatton, W. [Author, Reprint Author; E-mail: [email protected]]; Chalmers-Redman, R. [Author]; Tatton, N. [Author].
Institution
Department of Neurology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Annenburg 1470, Box 1137, New York, NY, 10029-6574, USA.
Title
Neuroprotection by deprenyl and other propargylamines: Glyceraldehyde-3-phosphate dehydrogenase rather than monoamine oxidase B.
Source
Journal of Neural Transmission. 110(5). May 2003. 509-515.
Abstract
Deprenyl and other propargylamines are clinically beneficial in Parkinson's disease (PD). The benefits were thought to depend on monoamine oxidase B (MAO-B) inhibition. A large body of research has now shown that the propargylamines increase neuronal survival independently of MAO-B inhibition by interfering with apoptosis signaling pathways. The propargylamines bind to glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The GAPDH binding is associated with decreased synthesis of pro-apoptotic proteins like BAX, c-JUN and GAPDH but increased synthesis of anti-apoptotic proteins like BCL-2, Cu-Zn superoxide dismutase and heat shock protein 70. Anti-apoptotic propargylamines that do not inhibit MAO-B are now in PD clinical trial.

````````````````````````````````````````
Author/Editor/Inventor
Schiffer, Wynne K. [Author, Reprint Author; E-mail: [email protected]]; Azmoodeh, Manijeh [Author]; Gerasimov, Madina [Author]; Volkow, Nora D. [Author]; Fowler, Joanna S. [Author]; Dewey, Stephen L. [Author].
Institution
Chemistry Department, Brookhaven National Laboratory, Upton, NY, 11973, USA.
Title
Selegiline potentiates cocaine-induced increases in rodent nucleus accumbens dopamine.
Source
Synapse (New York). 48(1). April 2003. 35-38.
Abstract
Selegiline has been proposed as a treatment for cocaine addiction and studies in humans suggest that it attenuates cocaine's reinforcing effects. Here we assessed the effects of selegiline treatment on cocaine-induced increases in nucleus accumbens (NAc) dopamine (DA) in freely moving rodents. Chronic treatment with selegiline (L-deprenyl, 0.25/mg/kg, 24 days) potentiated cocaine-induced increases in NAc DA from 350-600%. However, this enhanced response was abolished when animals were treated chronically with both cocaine and selegiline. Inasmuch as increases in NAc DA are associated with the reinforcing effects of cocaine, these results obtained in rodents suggest that MAO-A and -B inhibition may not be a suitable strategy to antagonize cocaine's reinforcing effects during cocaine detoxification. On the other hand, chronic selegiline treatment may improve DA deficits, which are thought to contribute to relapse through a decreased response to natural rewards.
`````````````````````````````````````````````````````
Author/Editor/Inventor
Dringenberg, Hans C. [Reprint author]; Rubenstein, Megan L. [Author]; Solty, Heidi [Author]; Tomaszek, Summer [Author]; Bruce, Alanna [Author; E-mail: [email protected]].
Institution
Department of Psychology, Queen's University, Kingston, ON, K7L 3N6, Canada.
Title
Electroencephalographic activation by tacrine, deprenyl, and quipazine: Cholinergic vs. non-cholinergic contributions
Source
European Journal of Pharmacology. 447(1). 28 June, 2002. 43-50.
Abstract
Drugs that stimulate central cholinergic transmission can induce activated, high frequency electroencephalographic (EEG) activity in rats. Monoaminergic enhancement also produces EEG activation, either by a direct stimulation of monoaminergic transmission in cortex, or a transsynaptic excitation of cholinergic projection neurons receiving excitatory monoaminergic afferents. We examined the degree of cholinergic involvement in EEG activation produced by monoaminergic and cholinergic drugs in rats. All animals were pretreated with 10 mg/kg reserpine and either 1 or 5 mg/kg scopolamine to abolish EEG activation. The acetylcholinesterase inhibitor tacrine (5-20 mg/kg) restored EEG activation in the low dose scopolamine group, but was less effective against the high scopolamine dose. The monoamine oxidase inhibitor deprenyl and the serotonergic receptor agonist quipazine restored EEG activation, an effect that was largely unaffected by different scopolamine doses. These results confirm that tacrine produces EEG activation by means of cholinergic stimulation. In contrast, activation produced by deprenyl or quipazine does not appear to be mediated by a transsynaptic excitation of cholinergic neurons and likely depends on a direct enhancement of cortical monoaminergic neurotransmission.

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Author/Editor/Inventor
Schiffer, Wynne K. [Author, Reprint Author; E-mail: [email protected]]; Azmoodeh, Manijeh [Author]; Gerasimov, Madina [Author]; Volkow, Nora D. [Author]; Fowler, Joanna S. [Author]; Dewey, Stephen L. [Author].
Institution
Chemistry Department, Brookhaven National Laboratory, Upton, NY, 11973, USA.
Title
Selegiline potentiates cocaine-induced increases in rodent nucleus accumbens dopamine.
Source
Synapse (New York). 48(1). April 2003. 35-38.
Abstract
Selegiline has been proposed as a treatment for cocaine addiction and studies in humans suggest that it attenuates cocaine's reinforcing effects. Here we assessed the effects of selegiline treatment on cocaine-induced increases in nucleus accumbens (NAc) dopamine (DA) in freely moving rodents. Chronic treatment with selegiline (L-deprenyl, 0.25/mg/kg, 24 days) potentiated cocaine-induced increases in NAc DA from 350-600%. However, this enhanced response was abolished when animals were treated chronically with both cocaine and selegiline. Inasmuch as increases in NAc DA are associated with the reinforcing effects of cocaine, these results obtained in rodents suggest that MAO-A and -B inhibition may not be a suitable strategy to antagonize cocaine's reinforcing effects during cocaine detoxification. On the other hand, chronic selegiline treatment may improve DA deficits, which are thought to contribute to relapse through a decreased response to natural rewards.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Djaldetti, R. [Reprint author]; Ziv, I. [Author]; Melamed, E. [Author]. The effect of deprenyl washout in patients with long-standing Parkinson's disease [Article] Journal of Neural Transmission. 109(5-6). May, 2002. 797-803.

Shoulson, Ira [Reprint author]; Oakes, David [Author]; Fahn, Stanley [Author]; Lang, Anthony [Author]; Langston, J. William [Author]; LeWitt, Peter [Author]; Olanow, C. Warren [Author]; Penney, John B. [Author]; Tanner, Caroline [Author]; Kieburtz, Karl [Author]; Rudolph, Alice [Author]; Parkinson Study Group [Author; E-mail: [email protected]]. Impact of sustained deprenyl (selegiline) in levodopa-treated Parkinson's disease: A randomized placebo-controlled extension of the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial [Article] Annals of Neurology. 51(5). May, 2002. 604-612.

Panahi, Merziah [Author]; Al-Tiraihi, Taki [Reprint author]. Morphometric evaluation of the neuroprotective effect of deprenyl on postaxotomic motor neuron losses [Article] Clinical Neuropharmacology. 25(2). March-April, 2002. 75-78.

Dong Wen-Xin [Reprint author]; Ni Xiang-Lian [Author; E-mail: [email protected]]. Norepinephrine metabolism in neuron: Dissociation between 3,4-dihydroxyphenylglycol and 3,4-dihydroxymandelic acid pathways [Article] Acta Pharmacologica Sinica. 23(1). January, 2002. 59-65

Kitani, K. [Reprint author]; Minami, C. [Author]; Maruyama, W. [Author]; Kanai, S. [Author]; Ivy, G. O. [Author]; Carrillo, M.-C. [Author; E-mail: [email protected]]. Common properties for propargylamines of enhancing superoxide dismutase and catalase activities in the dopaminergic system in the rat: Implications for the life prolonging effect of (-)deprenyl [Article] Journal of Neural Transmission. Supplementum. 60 2000. 139-156

Klegeris, Andis [Reprint author]; McGeer, Patrick L. [Reprint author]. R-(-)-deprenyl inhibits monocytic THP-1 cell neurotoxicity independently of monoamine oxidase inhibition [Article] Experimental Neurology. 166(2). December, 2000. 458-464

Schuler, A. [Reprint author]; Kalmanchey, R. [Author]; Barsi, P. [Author]; Somogyi, C. S. [Author]; Toros, I. [Author]; Varadi, I. [Author]; Kovacs, A. [Author]; Blau, N. [Author]. Deprenyl in the treatment of patients with tetrahydrobiopterin deficiencies [Article] Journal of Inherited Metabolic Disease. 23(4). June, 2000. 329-332.

Behan, W. M. H. [Author]; McDonald, M. [Author]; Darlington, L. G. [Author]; Stone, T. W. [Reprint author]. Oxidative stress as a mechanism for quinolinic acid-induced hippocampal damage: Protection by melatonin and deprenyl [Article] British Journal of Pharmacology. 128(8). Dec., 1999. 1754-1760

Kitani, Kenichi [Reprint author]; Kanai, Setsuko [Author]; Ivy, Gwen O. [Author]; Carrillo, Maria Cristina [Author]. Pharmacological modifications of endogenous antioxidant enzymes with special reference to the effects of deprenyl: A possible antioxidant strategy [Article] Mechanisms of Ageing & Development. 111(2-3). Nov., 1999. 211-221

Gallagher, I. M. [Author]; Clow, A. [Reprint author]; Jenner, P. [Author]; Glover, V. [Author]. Effect of long-term administration of pergolide and (-)-deprenyl on age related decline in hole board activity and antioxidant enzymes in rats [Article] Biogenic Amines. 15(3). 1999. 379-393

Alper, Gulinnaz [Reprint author]; Kulahcioglu Girgin, Ferhan [Author]; Ozgonul, Mert [Author]; Mentes, Gulriz [Author]; Ersoz, Biltan [Author]. MAO inhibitors and oxidant stress in aging brain tissue [Article] European Neuropsychopharmacology. 9(3). March, 1999. 247-252

Giladi, N. [Reprint author]; Honigman, S. [Author]; Hocherman, S. [Author]. The effect of deprenyl treatment on directional and velocity control of arm movement in patients with early stages of Parkinson's disease [Article] Clinical Neuropharmacology. 22(1). Jan.-Feb., 1999. 54-59

Melega, William P. [Reprint author]; Cho, Arthur K. [Author]; Schmitz, Debra [Author]; Kuczenski, Ronald [Author]; Segal, David S. [Author]. I-methamphetamine pharmacokinetics and pharmacodynamics for assessment of in vivo deprenyl-derived I-methamphetamine [Article] Journal of Pharmacology & Experimental Therapeutics. 288(2). Feb., 1999. 752-758

Shoulson, Ira [Reprint author]. DATATOP: A decade of neuroprotective inquiry [Article] Annals of Neurology. 44(3 SUPPL. 1). Sept., 1998. S160-S166.

Tarjanyi, Z. [Author]; Kalasz, H. [Reprint author]; Szebeni, G. [Author]; Hollosi, I. [Author]; Bathori, M. [Author]; Fuerst, S. [Author]. Gas-chromatographic study on the stereoselectivity of deprenyl metabolism [Article] Journal of Pharmaceutical & Biomedical Analysis. 17(4-5). Aug., 1998. 725-731.

Knoll, J. [Reprint author]. The history of (-)deprenyl the first selective inhibitor of type B monoamine oxidase [Article] Voprosy Meditsinskoi Khimii. 43(6). Nov.-Dec., 1997. 482-493.

Ekblom, J. [Reprint author]; Garpenstrand, H. [Author]; Tottmar, O. [Author]; Prince, J. A. [Author]; Oreland, L. [Author]. A cell culture model of cerebral ischemia as a convenient system to screen for neuroprotective drugs [Article] Journal of Neural Transmission. Supplementum. 52(0). 1998. 93-98.

40. Gil, R. [Author]; Creange, A. [Author]; Degos, J.-D. [Author]; Adle-Biassette, H. [Author]; Gray, F. [Author]. Extra-pyramidal syndrome, hallucinations and dementia in a 70-year-old woman [Article] Revue Neurologique (Paris). 153(6-7). July, 1997. 440-447

Lamensdorf, I. [Author]; Finberg, J. P. M. [Reprint author]. Reduced striatal tyrosine hydroxylase activity is not accompanied by change in responsiveness of dopaminergic receptors following chronic treatment with deprenyl [Article] Neuropharmacology. 36(10). Oct., 1997. 1455-1461
Wei, Qize [Author]; Jurma, Octavian P. [Author]; Anderson, Julie K. [Reprint author]. Increased expression of monoamine oxidase-B results in enhanced neurite degeneration in methamphetamine-treated PC12 cells [Article] Journal of Neuroscience Research. 50(4). Nov. 15, 1997. 618-626

Mukherjee, Jogeshwar [Reprint author]; Yang, Zhi-Ying [Author]. Evaluation of monoamine oxidase B inhibition by fluoxetine (Prozac): An in vitro and in vivo study [Article] European Journal of Pharmacology. 337(1). Oct. 15, 1997. 111-114
Click to expand...
 
Would its MAO inhibiting qualities mean it's useful for making oral doses of DMT effective?
 
I'm going to give selegiline another go, and a serious one.

Admittedly I'll be combining with other stuff, but we'll see how my energy levels are affected etc.

I'll be taking the following per day
5mg selegiline
1800mg piracetam
500mg choline bitartrate
swisse mens multivitamin (highly recommend them!)
500mg l-phenylalanine morning (and more in the arvo)
1.2g lecithin
ginkgo bilboa tablets (the ones from blackmores).
blackmore's B vitamin tablet.
4.25 mg hydergine

need to cram heh
 
Last edited:
Update: Been taking the above combo minus the ginkgo bilboa every day since saturday, and I do have to say that I feel more clearheaded...

My memory also seems to be improved... i've been doing law notes, and i can seem to remember the cases much easier... I don't have to memorise them, as its an open book exam, but I seem to be able to recall the case names and what they are about much much more easily... (I'm not trying to memorise at all)

My motivation to study is about the same it always was, but I feel like my focus has improved... managed to write 9000 words of notes yesterday :D

Will persist and see what happens.
 
I feel like I've got more energy overall to be honest.... I've been sleeping a little less, though not significantly so.

It's really weird, I go through maybe a 20 minute patch of feeling somewhat tired every few hours, and then strangely wake right back up again? somewhat odd....

Went out drinking last night, got to bed at 2:30am or so... was up at 6:30 this morning and I don't really feel tired.. haven't had any caffeine either
 
Vilocidex: how has the piracetam/choline combo worked out? Any potentiation? I guess it would be hard to notice considering the smorgasboard of other nootropics youre taking =D

I just had a question about selegiline and speed. P_D you mentioned that it could be a bad combo to combine selegeline and ADD meds and Ive read that potentiation of amps can occur. I guess Im just pretty keen to contionue with the selegiline/l-phen combo....... how serious could it be to mix these two regularly. Im currently only on 5mg dex in the morn and arvo.

I totally respect your last comment P_D...Im just interested if there is anyway it can be done with caution.
 
It's kind of hard to say what's coming from what, on account of the combo like you said. It's been 1.5 weeks now and I feel like the benefits are *still* increasing :D

Re the speed + selegiline combo, its kindof hard to say what the effect will be as dopamine has an alternate metabolic pathway through COMT (Catetcholamine-O-MethylTransferase, i *think*)... i know very little about that system, and all the percentages involved. I'd be inclined to be extremely cautious.
 
So if someone felt depressed and was having difficulty with clear headedness and memory would deprenyl be something worth trying to obtain and in conjuction with something else or by itself
 
^^ i think it would be worthwhile trying one of the other more mainstream antidepressants first. at doses normally prescribed as an antidepressant, the MAOi diet applies.
and that sounds no fun at all.

plus if you want to do drugs, there are other much safer options.
 
What would be recomended to someone with mainly with memory recall being the problem thats what seems to be feeding the depression and destroying confidence at the same time.

Getting lost in the middle of a conversation forgeting what your talking about quite often and haven't had alot of drugs lately.

Feeling really scattered.
I have heard stories about doctors proscribing wrong medications causing even more problems so i'm trying to obtain as much info on what might be a good solution.

I have it a guess that I may of done the damage during weekly pill use over extended time any recomendations would be appreciated.
 
I'm coming up to my exams now and I have to say I think my nootropic splurge has been worth it...

in the last two days I've managed to learn and memorise the best part of 160 pages of statistical physics... admittedly i'm not memorising anything word for word, but there's a lot of derivations with a lot of finicky steps that are quite confusing.. Two days before that I revised a similar amount of quantum mechanics, and I appear to have retained *most* of it.

I should have learnt this subject right from the start, but the lecturer was pretty poor and I hate anything involving statistics...

re Selegiline
It's rather weird. You know the feeling when you know something? When someone asks you a question and you know you know the answer to it? You feel confident in your knowledge? I don't have that feeling. To be honest I feel like I know very little, but then when i actually go to do it I remember huge slabs of it... it's rather odd.

I've been taking 5mg/day of selegiline about 15 mins after breakfast (two pieces of toast, milk, vita brits).... I spread promite on my toast (high in tyramine) and have experienced nothing remotely resembling a hypertensive crisis... no headaches, sweating, dizziness etc.

500mg l-phenylalanine seems to work, 1g seems to work better.... I don't really feel that selegiline gives a "clear-headed" feeling so much... I've still been using caffeine tablets where appropriate etc.

I have noticed that in darker rooms my pupils are larger than they normally would be. Not completely dilated, but still quite large. At night I get substantial halos (white-blue) around street lights, and around other lights. Looking at bright nights in the street at night I get a mild version of the "overexposed" look that you get from pills, where there's this pure white in the centre.

I had hoped that selegiline might do something for my tiredness, but alas it has not. The first day I took it I noticed a stimulant effect, but it declined thereafter (even with phenylalanine).

Summary: I found selegiline to be a useful adjunct to piracetam + choline supplementation. It's not some miracle drug that bestows an infinite learning capacity, but it does seem to work.

Comments re Hydergine
I'm not sure what hydergine has done in this mix... I've only take it some days, and I noticed that on some of those days I felt somewhat tired... I was awake, but my brain felt sluggish. I cannot say whether this is the Hydergine or merely some uncorrelated effect from my sleeping hours or caffeine withdrawl etc, but I do have to say its odd. I used it today and felt more clearheaded... used it yesterday and felt somewhat dull.

I may try this again in future, though I can't say when.

Now its over?
My main concern now that I'm about to stop the selegiline is when I can next do pills, to be honest... The best studies I can find put the mean time to plasma MAO-B return at around 240ish hours, up to 300 in people who have been taking it for multiple months... I'll keep taking phenylalanine for the next week or two and observe what happens to my eyes. I intend to leave at least 8 or 9 days between now and taking pills, and will see how I go in the meantime.
 
Thanks for the details VeloxideX. While we can never totally remove the element of subjectivity from a self monitored trial such as this, it would be interesting to compare notes with someone older who used selegiline.

The endogenous levels of MAOB between you at 21, and me at over twice that age would be considerably different. At 21 I too had a pretty much photographic memory for most things (it had to be either science, music, philosophy or magic though.. ;)). These days, although I can usually nut things out, completely new concepts do often take longer to gel, no doubt about it, and there's a lot more attention required to avoid error or omission :(

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BT's super-auto-proof-reading-reminder service... ;)
 
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Grr for MAOB levels rising as you get older. I too can remember heaps of stuff scientific etc, but don't try and get me to memorise anything history wise or arty or I'll die heh

I wonder what research is like with CREB... I've heard somewhere on here that people with true photograph memories show overexpression of CREB, and that there's research going on into whether its possible to artificially elevate CREB levels in "normal" people...
 
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