58 replies to this topic

[enigma]

Id be interested to learn what has worked best for others.

[spider]

For me, both Picamilon and Vinpocetine are great (vasodilator) nootropics, but I do not notice/like the effects of ginko-biloba and Hydergine.

[Shepard]

My favorite is a combination of vinpocetine and ginkgo biloba.

[REGIMEN]

My vote was for Picamilon. Best effects for me ("creativity enhancing"). Gingko and Vinpo just give a boost to the senses it seems; too normal since I can get the same effects by doing some morning breathing/yoga.

da_sense, I've had bad reactions when taking multiple vasodilators. I'm fine if I take Picamilon or these grocerystorebrand Gingko/Vinpo tabs separately(not on the same day), but if I take both I get seriously irritable and can't focus. Maybe you're doing just fine in that department with no need for vasodilators. Healthy lifestyle? All the better.

[lemon]

Picamilion is slightly toxic.

Hydergine boosts endogenous superoxide dismutase and catalase levels in the brain... absolutely and unequivically priceless !!

[lemon]

As a side bar... very very few compounds can boost endogenous antioxidant enzymes and when you know what they are you should'nt be skipping over them for lesser dietary antioxidants including grape seed PCOs or EGCGs.

You're endogenous antioxidant enzymes will always dominate free radical containment throughout your body.

[thumb]

[johnmk]

Picamilion is slightly toxic.

Hydergine boosts endogenous superoxide dismutase and catalase levels in the brain... absolutely and unequivically priceless !!

Doesn't deprenyl do some of that too?

[lemon]

Deprenyl is readily recognized as a selective MAO-B inhibitor and not really as an endogenous antioxidant enzyme promoter.

Hydergine, on the other hand, is administered in hospitals for brain cell protection in trauma to protect against oxygen deprivation and stop massive free radical cascading.

(of course not in the U.S. unless specifically requested. Blame our FDA for only approving it for dementia).

[wannafulfill]

Deprenyl is readily recognized as a selective MAO-B inhibitor and not really as an endogenous antioxidant enzyme promoter. 

Hydergine, on the other hand, is administered in hospitals for brain cell protection in trauma to protect against oxygen deprivation and stop massive free radical cascading. 

(of course not in the U.S. unless specifically requested.  Blame our FDA for only approving it for dementia).

well... there's these and others that show that deprenyl is:

1: Mech Ageing Dev. 2002 Apr 30;123(8):1087-100. Related Articles, Links


Why (--)deprenyl prolongs survivals of experimental animals: increase of anti-oxidant enzymes in brain and other body tissues as well as mobilization of various humoral factors may lead to systemic anti-aging effects.

Kitani K, Minami C, Isobe K, Maehara K, Kanai S, Ivy GO, Carrillo MC.

National Institute for Longevity Sciences, 36-3, Gengo, Morioka-cho, Obu-shi, Aichi 474-8522, Japan. kitani@nils.go.jp

(--)Deprenyl, a monoamine oxidase B (MAO B) inhibitor is known to upregulate activities of anti-oxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) in brain dopaminergic regions. The drug is also the sole chemical which has been repeatedly shown to increase life spans of several animal species including rats, mice, hamsters and dogs. Further, the drug was recently found to enhance anti-oxidant enzyme activities not only in brain dopaminergic regions but also in extra-brain tissues such as the heart, kidneys, adrenal glands and the spleen. We and others have also observed mobilization of many humoral factors (interferone (INF)-gamma, tumor necrosis factor (TNF)-alpha, interleukine (IL)-1beta,2,6, trophic factors, etc.) and enhancement of natural killer (NK) cell functions by (-)deprenyl administration. An apparent extension of life spans of experimental animals reported in the past may be better explained by these new observations that (-)deprenyl upregulate SOD and CAT activities not only in the brain but also in extra-brain vital organs and involve anti-tumorigenic as well as immunomodulatory effect as well. These combined drug effects may lead to the protection of the homeostatic regulations of the neuro-immuno-endocrine axis of an organism against aging.

Publication Types:
Review
Review, Tutorial

PMID: 12044958 [PubMed - indexed for MEDLINE]

2: J Neural Transm. 2005 Jun 15; [Epub ahead of print] Related Articles, Links


Effects of selegiline on antioxidant systems in the nigrostriatum in rat.

Takahata K, Shimazu S, Katsuki H, Yoneda F, Akaike A.

Research Institute, Fujimoto Pharmaceutical Corporation, Osaka, Japan.

Selegiline, a therapeutic agent of Parkinson's disease, is known to have neuroprotective properties that may involve its regulatory effects on antioxidant enzymes. We evaluated effects of selegiline on activities of catalase (CAT), Cu,Zn-superoxide dismutase (SOD1) and Mn-SOD (SOD2) in the striatum, cortex and hippocampus of 8- and 25-week-old rats, and on SOD activities and glutathione levels in mesencephalic slice cultures. Selegiline (2 mg/kg) significantly increased CAT and SOD2 activities in the striatum, but not in the cortex and hippocampus, of 25-week-old rats. In contrast, selegiline failed to increase CAT and SOD activities in three brain regions of 8-week-old rats, whereas L: -dopa significantly increased SOD1 activity in the striatum. In slice cultures, selegiline increased SOD1 and SOD2 activities with a maximal effective concentration of 10(-8) and 10(-10) M, respectively. Moreover, selegiline significantly increased glutathione level. These results suggest that selegiline can decrease oxidative stress in nigrostriatum by augmenting various antioxidant systems, each of which responds optimally to different concentrations of selegiline.

PMID: 15959853 [PubMed - as supplied by publisher]

3: Physiol Res. 2005 May 24; [Epub ahead of print] Related Articles, Links


Deprenyl and the relationship between its effects on spatial memory, oxidant stress and hippocampal neurons in aged male rats.

Kiray M, Bagriyanik HA, Pekcetin C, Ergur BU, Uysal N, Ozyurt D, Buldan Z.

Department of Histology&Embryology, Dokuz Eylul University Medical School, Balcova, Izmir 35340, Turkey. muge.kiray@deu.edu.tr.

The oxidative stress may play a major role on the aging process and associated cognitive decline, therefore antioxidant treatment may alleviate age-related impairment in spatial memory. Cognitive impairment could also involve the age-related morphological alterations of hippocampal formation. The aim of this study is to examine the relationship between the effects of deprenyl, an irreversible monoamine-oxidase B inhibitor, on spatial memory by oxidant stress and total number of neurons in the hippocampus CA1 region of aged male rats. In this study 24 months old male rats were used. Rats were divided into control and deprenyl groups and injected for 21 days. Learning experiments were performed for six days in the Morris water maze. Spatial learning was significantly better in deprenyl-treated rats compared to saline-treated rats. Deprenyl treatment elicited a significant decrease of lipid peroxidation in prefrontal cortex, striatum and hippocampus regions and a significant increase of glutathione peroxidase activity in the prefrontal cortex and hippocampus. It was observed that deprenyl had no effect on the superoxide dismutase activity. The total neuron numbers in the hippocampus CA1 region were significantly higher in the deprenyl group than in the control group. In conclusion, we demonstrated that deprenyl increases spatial memory performance in aged male rats and this increase may be related to suppression of lipid peroxidation and alleviation of age-related decrease of the number of neurons in the hippocampus. The results of such studies may be useful in pharmacological modification of aging process.

PMID: 15910165 [PubMed - as supplied by publisher]


In terms of arguing that it does not promote systemic antioxidant systems, I guess you could point to parts of this, however:

1: Brain Res. 2002 Oct 25;953(1-2):1-11. Related Articles, Links


Effects of short- and long-term (--)-deprenyl administration on mRNA for copper, zinc- and manganese-superoxide dismutase and glutathione peroxidase in rat brain.

Kunikowska G, Gallagher I, Glover V, Clow A, Jenner P.

Neurodegenerative Diseases Research Centre, Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas School of Biomedical Sciences, Hodgkin Building, Guy's Campus, London SE1 1UL, UK.

The effect of short-term (3 weeks, 2 mg/kg day) and long-term (12 and 20 months, 0.5 mg/kg day) administration of (-)-deprenyl on the mRNA expression of three neuroprotective enzymes in subdivisions of rat basal ganglia was investigated. In situ hybridisation histochemistry with oligodeoxynucleotide probes was used to measure levels of copper, zinc superoxide dismutase (Cu,Zn-SOD), manganese superoxide dismutase (Mn-SOD), and glutathione peroxidase (GPX) mRNA. The 3-week administration of (-)-deprenyl caused a significant increase in Cu,Zn-SOD mRNA in the nucleus accumbens (NA) (P<0.05), striatum (CP) (P<0.01), and globus pallidus (GP) (P<0.05), but had no effect on Mn-SOD or GPX mRNA levels throughout basal ganglia. In rats which received (-)-deprenyl for 12 months, there was a significant increase in Mn-SOD mRNA in the NA, CP, GP, and substantia nigra (SN) (all P<0.05); there were no changes in either Cu,Zn-SOD or GPX mRNA. Except for the significant increase in Cu,Zn-SOD mRNA in SN pars compacta (SC) (P<0.05), by 20 months there were almost no differences between (-)-deprenyl-treated and age-matched control animals that had received equivalent injections of saline. We conclude that (-)-deprenyl administration can induce mRNA expression for both forms of SOD, but the effects are variable and not sustained over 20 months.

PMID: 12384232 [PubMed - indexed for MEDLINE]


In terms of SOD, bacopa appears to be king.

[dirac]

hmm i happen to be in a group where vasolidators do not help me, i have a feeling they make my cognition and mind state worse...could this be possible?
i like coffeine, it's constrictor...maybe i'm alien?

I must concur with the statement that "vasodilators do not help me."
I find that taking one gives me headaches and other not so fun things, as I recall, which seems to be unfortunate in light of the putative benefits that are derived from taking them.

[REGIMEN]

lemon , where is a linked source backing your statement of Picamilon as "slightly toxic"? Anyone reading that will now have to go scrounging for the source of that claim in which the difficulty will be compounded by the numerous spellings of said drug (c-k, n-ne, etc.) Let's be a little more vigilant, now, especially if on Hydergine. If only for posterity's sake.

[lemon]

liplex: Niacin.

[lemon]

da_sence,

Titrate back down to 1mg and you should be fine.

[LifeMirage]

Picamilion is slightly toxic.

Picamilon is a very safe compound that does not contain Niacin. It is a chemical combination of GABA and an analog of Niacin.

Picamilon produces no allergenic, teratogenic, embryotoxic or carcinogenic effects. On this basis, the pharmacological committee of the Ministry of the Health (Russia) recommended clinical trials of Picamilon for cerebrovascular disturbances, as a daytime tranquilizer, as a stimulant in depressive and asthenic (weakening) states, and to improve physical and mental working capacity. Picamilon was studied in a large number of scientific facilities within Russia. The total number of patients under observation was 984. Picamilon tablets were prescribed two to three times a day at a dose of 0.02 to 0.05 grams, and in a daily dose of 0.04 to 0.3 grams.

[REGIMEN]

lemon,
Niacin..toxic?

There are two pharmaceutical grade multivitamin favorites on this forum and they both contain an above RDA value of Niacin.

I thought source linking was common courtesy here, especially for claiming something as a malfactor.
The weight of the ignorant can be a burden. Sorry.

[LifeMirage]

Hydergine and Vincamine works best for me.

[lemon]

Eksp Klin Farmakol. 2003 Jul-Aug;66(4):43-6. Related Articles, Links


[Preclinical prognosis of pyracetam and picamilon safety based on acute toxicity data]

[Article in Russian]

Bugaeva LI, Spasov AA, Verovskii VE, Iezhitsa IN.

Institute of Pharmacology, Volgograd State Medical Academy, pl. Pavshikh Bortsov 1a, Volgograd, 400066 Russia.

A comparative acute toxicity test of the nootropic drugs piracetam and picamilon was performed on rats. The study was based on the principles of integral evaluation of the drug effect upon the functional and behavioral state of animals. It was found that the conventional therapeutic index does not coincide with the actual therapeutic activity range. Piracetam and picamilon, while exhibiting significantly different toxicity, are characterized by approximately equal ranges of the therapeutic activity.

PMID: 14558352 [PubMed - indexed for MEDLINE]

Pikamilone is not a nootropic because it is somewhat toxic (albeit slight, but toxic none-the-less). Life extensionists should not be taking it chronically because you're, in effect, robbing Peter to pay Paul (getting a niacin flush at the expence of long term damage).

[jeromewilson]

getting a niacin flush at the expence of long term damage

I've never experienced anything like a Niacin flush when taking Picamilone.

Piracetam and picamilon, while exhibiting significantly different toxicity

This could be taken to imply that picamilone is toxic, but I'm really just confused...

[LifeMirage]

Unfortunately many people cannot proper interpret studies.

In simpler terms:

The mice study was designed to determine the known toxic doses of Picamilon & Piracetam (which is remarkable high and well above the doses used in human studies) for comparison purposes…they were found to induce a toxic level at similar mg per kg.

If as you claim Picamilon is toxic then Piracetam would be equally so….which is just not the case.

As far as there being niacin in Picamilon there simply isn’t any.

I will agree with you as far as it not being a true nootropic as far as its strength in enhancing cognition (memory, processing, etc..) goes compared to other nootropics…I consider it a weak or mild nootropic because it does have some effect on cognition.

I strongly suggest reading Picamilon Research in the Nootropic Research forum.

Yours In Health

[johnmk]

Are niacin flushes damaging?

[LifeMirage]

If you have liver damage taking high doses of Niacin (over 50-100 mg) is probably not a good idea...but heathly people can take up to 500 mg daily without causing liver damage. Some people are sensitive to it at any dose and it does make the liver work harder in high doses.

[enigma]

Presumably, more people have taken Vinpocetine than Picamilon, so, perhaps Picamilon would be even more preffered if this poll was not bias (everyone had tried everything), too bad there is not a great amount of literature in English on Picamilon, im a little concerned with its mild Mao-A inhibiting effect.

[FunkOdyssey]

Favorite vasodilator? Tadalafil.

[spaceistheplace]

Vinpocetine by far.

It only takes 5mg for me to feel it all day. Any more than that gives me a headache.

[Rags847]

Favorite vasodilator? Tadalafil.

Ha! Ha! Ha!
Cialis rules!!!

Keeps lower back problems from interfering.

[Karomesis]

NtBHA

[pycnogenol]

NtBHA

I'm thinking about adding ntBHA to my stack. Do you still get your supply at GeroNova?

[Advanc3d]

My favorite is a combination of vinpocetine and ginkgo biloba.

has that ever caused u hypotension followed by headaches?
when ever i just take vinpocetine it feels like i sniffed petrol or something, my head is going to explode@!