2626 replies to this topic

[canz]

Let us know how you do on this particular brand.

What's the best source people have found for forskolin? I bought some 95% extract off of bodybuilding.com the other day:

http://www.bodybuild...rts/cbolic.html

Related to the previous post, the dosage on that 95% extract for fat burning/muscle building purposes is 25mg forskolin 2x daily, which is a lot more than most people in this thread are taking. We are potentiating the effect with pde inhibitors, but I am very interested in trying to figure out what causes the tiredness that some people have reported. Presumably it doesn't make most people tired when they take it as labeled without pde inhibition, or it wouldn't be a good bodybuilding supplement.

[hephaestus]

Has anyone noticed a difference between supplementing phenylalanine vs tyrosine as a neurotransmitter precursor? Increased cAMP increases tyrosine hydroxylase transcription which should cause dopamine to be produced more quickly since it is the rate limiting enzyme in getting from tyrosine to DA. If you are just supplementing phenylalanine you might not be able to keep up with the increased tyrosine usage since phenylalanine hydroxylase transcription is unaffected by cAMP, as far as I know.

I have a poor background in biology but perhaps this could be related to the fatigue?

https://en.wikipedia...lase#Regulation

Tyrosine hydroxylase activity is regulated chronically (days) by protein synthesis.

[hephaestus]

Let us know how you do on this particular brand.

What's the best source people have found for forskolin? I bought some 95% extract off of bodybuilding.com the other day:

http://www.bodybuild...rts/cbolic.html

Related to the previous post, the dosage on that 95% extract for fat burning/muscle building purposes is 25mg forskolin 2x daily, which is a lot more than most people in this thread are taking. We are potentiating the effect with pde inhibitors, but I am very interested in trying to figure out what causes the tiredness that some people have reported. Presumably it doesn't make most people tired when they take it as labeled without pde inhibition, or it wouldn't be a good bodybuilding supplement.

Just finished emptying the capsules, it comes out to about $12/gm 95% forskolin, so not actually much more than zr wants to repackage the 98%. Where are you ordering it from zr? I thought I remembered seeing a link in here somewhere but I couldn't find it.

[gizmobrain]

PhytoPharmacon. They don't do online orders; you have to mail them a check. Their prices get significantly cheaper the more you order, but I'd never be able to use 10 grams of the 98% extract by myself.

If we organized a group buy of 10 grams or more, it'd save us about $10 a gram. I have a scale, and can redistribute them into 1/2 oz jars like these and ship them within the US. I could even buy a pack of the microdosing scoops (10-15mg) and include one in each package, if desired.

Edited by zrbarnes, 10 August 2012 - 12:43 AM.

[hephaestus]

What is the price at 10 grams? I have a friend interested and I think we could probably do at least 5, depending on price.

[gizmobrain]

Straight from PhytoPharmacon, it's $35 shipped for 1 gram, and $85 shipped for 10 grams.

If I get any interest in a group buy, I could buy 10 grams, and repackage it for $10 a gram + actual cost of shipping to you (~$2-6 depending how you want it shipped). That would cover the containers, scoop, and packaging (and a nickle for my time, ).

Anyway, we should probably move this discussion to a PM. If anyone else is interested, just let me know.

Edited by zrbarnes, 10 August 2012 - 09:21 AM.

[abelard lindsay]

I found out today that my sleepiness on non-stack days can be largely alleviated by supplementing with l-phenylalanine. Perhaps this is related to upregulation of Tyrosine Hydroxylase?

Hmm..let's see what's new with cAMP and Tyrosine Hydroxylase.

http://www.ncbi.nlm....pubmed/22738763

Deficiency of catecholamine syntheses caused by downregulation of phosphorylation of tyrosine hydroxylase in the cerebral cortex of the senescence-accelerated mouse prone 10 strain with aging.
...
The present study demonstrated that a decline in DA and NE concentrations was observed in the cerebral cortex of SAMP10 with aging, and this decrease of catecholamine levels was caused by impairment of their synthetic pathway. These impairments are considered to be caused by downregulation of TH phosphorylation at Ser40 as a result of PKA deficiency. The present study suggests that the decline of learning and memory abilities of SAMP10 is caused by a decrease in catecholamine synthesis in the cerebral cortex with aging.
...

So these mice, who are genetically engineered to be prone to aging faster than other mice have deficient Tyrosine Hydroxylase which causes them to have a deficiency of catecholamines and thus a decline in learning and memory abilities.


http://www.ncbi.nlm....pubmed/22293035

Modulatory effects of sesamin on dopamine biosynthesis and L-DOPA-induced cytotoxicity in PC12 cells.
Zhang M, Lee HJ, Park KH, Park HJ, Choi HS, Lim SC, Lee MK.


Source
College of Pharmacy and Research Center for Bioresource and Health, Chungbuk National University, 52, Naesudong-ro, Heungduk-gu, Cheongju 361-763, Republic of Korea.


Abstract
The effects of sesamin on dopamine biosynthesis and L-DOPA-induced cytotoxicity in PC12 cells were investigated. Sesamin at concentration ranges of 20-75 μM exhibited a significant increase in intracellular dopamine levels at 24 h: 50 μM sesamin increased dopamine levels to 133% and tyrosine hydroxylase (TH) activity to 128.2% of control levels. Sesamin at 20-100 μM rapidly increased the intracellular levels of cyclic AMP (cAMP) to 158.3%-270.3% of control levels at 30 min. At 50 μM, sesamin combined with L-DOPA (50, 100 and 200 μM) further increased the intracellular dopamine levels for 24 h compared to L-DOPA alone. In the absence or presence of L-DOPA (100 and 200 μM), sesamin (50 μM) increased the phosphorylation of TH, cAMP-dependent protein kinase (PKA), and cAMP-response element-binding protein (CREB), as well as the mRNA levels of TH and CREB for 24 h, an effect which was reduced by L-DOPA (100 and 200 μM). In addition, 50 μM sesamin exhibited a protective effect against L-DOPA (100 and 200 μM)-induced cytotoxicity via the inhibition of reactive oxygen species (ROS) production and superoxide dismutase reduction, induction of extracellular signal-regulated kinase (ERK)1/2 and BadSer112 phosphorylation and Bcl-2 expression, and inhibition of cleaved-caspase-3 formation. These results suggested that sesamin enhanced dopamine biosynthesis and L-DOPA-induced increase in dopamine levels by inducing TH activity and TH gene expression, which was mediated by cAMP-PKA-CREB systems. Sesamin also protected against L-DOPA (100-200 μM)-induced cytotoxicity through the suppression of ROS activity via the modulation of ERK1/2, BadSer112, Bcl-2, and caspase-3 pathways in PC12 cells. Therefore, sesamin might serve as an adjuvant phytonutrient for neurodegenerative diseases.

So Sesamin is a cAMP increaser, like forskolin and increases phosphorylation of CREB and is a brain anti-oxidant! Is Sesamin the new Forskolin? Wow!

Sesamin is a body building supplement that's been around for some time, so this should be easy to try out.

[hephaestus]

Totally agree about the phenylalanine, I also supplement some n-acetyl-tyrosine. Elevated cAMP seems to cause DA to be synthesized very quickly from nat, I actually feel a bit of a body buzz sometimes. Slightly worried about the buildup of dopamine metabolites over the long term. I also take rhodiola so that combined with the COMT inhibition of quercetin should mitigate this to some degree. Any idea if you can build up too much l-DOPA this way? My understanding is that tyrosine hydroxylase is always the rate limiting enzyme, so it shouldn't be an issue?

Edited by hephaestus, 12 August 2012 - 02:37 AM.

[abelard lindsay]

Totally agree about the phenylalanine, I also supplement some n-acetyl-tyrosine. Elevated cAMP seems to cause DA to be synthesized very quickly from nat, I actually feel a bit of a body buzz sometimes. Slightly worried about the buildup of dopamine metabolites over the long term. I also take rhodiola so that combined with the COMT inhibition of quercetin should mitigate this to some degree. Any idea if you can build up too much l-DOPA this way? My understanding is that tyrosine hydroxylase is always the rate limiting enzyme, so it shouldn't be an issue?

The mechanisms of L-DOPA supplementation leading to toxicity in Parkinsons patients is a bit of a mystery, especially since the ongoing Parkinsons neuropathology complicates investigating it a bit. The theory that L-DOPA is responsible for accelerated neurodegeneration is even somewhat controversial. Dopamine converted by MAO-B to DOPAL and the inability to clear the DOPAL is suggested to be the cause of the Parkinsons pathology which is why MAOB inhibitors are regularly prescribed for Parkinsons issues, but this is not the confirmed mechanism of action for L-DOPA toxicity. L-DOPA makes up for the inhibition of tyrosine hydroxylase caused by Parkinsons pathology.

L-DOPA converts directly into dopamine via DOPA decarboxylase in the presence of vitamin B6. So far so good. From here there are two ways the dopamine degrades, via COMT and MAOB.

Does a COMT inhibitor make the L-DOPA problem worse?

This study says "meh":
http://www.ncbi.nlm....ubmed/19058133/

Dyskinesia was observed in 11 (5.3%) subjects in the LCE group and 16 (7.4%) in the LC group (P = 0.367).
...
LCE provided greater symptomatic benefit than LC and did not increase motor complications.

Does A MAOB inhibitor make things worse?

This study says yes..sort of... Some symptoms got worse, others got better.
http://www.ncbi.nlm....pubmed/12112107

Levodopa-treated Parkinson's disease patients who had been treated with deprenyl for up to 7 years, compared with patients who were changed to a placebo after about 5 years, experienced slower motor decline and were more likely to develop dyskinesias but less likely to develop freezing of gait.

So by upregulating tyrosine hydroxylase are we creating too much L-DOPA? How much is that enzyme being upregulated? If so, could it possibly metabolize enough tyrosine into L-DOPA to cause problems? I don't know. I don't think upregulating tyrosine hydroxylase via cAMP has never been tried as a treatment for Parkinsons because nobody in the traditional scientific community has even looked at it since 1984. The army looked at it a while back according to Wikipedia and got promising results.

What about studies on healthy rats given L-DOPA? This would get all the confusion caused by the on-going Parkinson's pathology in most L-DOPA studies out of the way.

http://www.ncbi.nlm..../pubmed/8479601

L-dopa, the major treatment for Parkinson's disease (PD), depletes S-adenosyl-L-methionine (SAM). Since SAM causes PD-like symptoms in rodents, the decreased efficacy of chronic L-dopa administered to PD patients may result from a rebound increase in SAM via methionine adenosyl transferase (MAT), which produces SAM from methionine and ATP. This was tested by administering intraperitoneally saline, or L-dopa to mice and assaying for brain MAT activity. As compared to controls, L-dopa (100 mg/kg) treatments of 1 and 2 times per day for 4 days did not significantly increase MAT activity. However, treatments of 3 times per day for 4 and 8 days did significantly increase the activity of MAT by 21.38% and 28.37%, respectively. These results show that short interval, chronic L-dopa treatments significantly increases MAT activity, which increases the production of SAM. SAM may physiologically antagonize the effects of L-dopa and biochemically decrease the concentrations of L-dopa and dopamine. Thus, an increase in MAT may be related to the decreased efficacy of chronic L-dopa therapy in PD.

So the theory is that L-DOPA depletes SAM(S-adenosyl-L-methionine) which causes MAT to upregulate which causes more SAM which causes decreased concentrations of L-Dopa and Dopamine. Thereby losing its effectiveness in Parkinsons disease.

Then there's the other theory that it downregulates DAT, but only in rats first injected with a parkinsons causing neurotoxin, so again the confound of the Parkinsons pathology.

And then there's this study.

http://www.ncbi.nlm..../pubmed/6147392

Nigrostriatal dopaminergic neurons remain undamaged in rats given high doses of L-DOPA and carbidopa chronically.
Perry TL, Yong VW, Ito M, Foulks JG, Wall RA, Godin DV, Clavier RM.

Abstract
Rats were fed maximally tolerated doses of L-3,4-Dihydroxyphenylalanine (L-DOPA) and carbidopa daily for 120 days in order to achieve a sustained elevation in brain dopamine levels. Some animals were also given buthionine sulfoximine, a gamma-glutamylcysteine synthetase inhibitor, in an unsuccessful effort to reduce brain glutathione contents. L-DOPA- and carbidopa-treated animals displayed no behavioral changes suggestive of nigrostriatal dopaminergic neuronal loss. When sacrificed 60 days after L-DOPA treatment ended, all rats had normal tyrosine hydroxylase activities and dopamine contents in their striata, and cell counts were normal in the substantia nigra. It therefore seems unlikely that a model of Parkinson's disease, suitable for exploring the etiological importance of glutathione deficiency, can be produced in rats merely by administering the largest tolerable doses of L-DOPA.

Another study says that the L-DOPA itself causes apoptosis to cell cultures and says that it doesn't show up in vivio because apoptotic neurons are rapidly disposed of. Still, it's a culture study and not in vivio and the in vivio study said it did not cause any measurable signs of neurodegeneration.

Given all this confusion and controversy, I'm going to stick to L-Phenylalanine supplementation because that isn't converted directly to L-DOPA by Tyrosine Hydroxylase and there's a rate limiting enzyme that limits its rate of conversion to Tyrosine: Phenylalanine hydroxylase.

Here's one more interesting study:

http://www.ncbi.nlm....pubmed/22583428

CNS Neurol Disord Drug Targets. 2012 Jun 1;11(4):450-5.
Current status of tyrosine hydroxylase in management of Parkinson's disease.
Feve AP.

Source
Neurology Department, Parkinson Unit, Leopold Bellan Hospital, 19-21 rue Vercingetorix, 75014 Paris, France. afeve@aol.com.

Abstract

Tyrosine hydroxylase (TH) is the rate limiting enzyme responsible for converting tyrosine to L-DOPA in the dopamine synthesis pathway. The pathophysiology of Parkinson's disease (PD) is largely due to the nigrostriatal dopaminergic system, with a decrease in TH activity, TH synthesis and TH mRNA in the striatum of PD and animal experimental models. TH is thus one of the main targets for gene therapy in PD. TH activity variations during L-DOPA and new antiparkinsonian treatments have been extensively studied. Pharmacological trials with neuroprotective treatments could modify these variations, suggesting a direct involvement of TH cells in the neurodegenerative process. α- Synuclein, the main component of Lewy bodies regulates the production of dopamine through its interaction with TH. Over-expression of α-synuclein reduces the levels of TH mRNA and protein in the brain and in this way links the histological description of PD and its pathological biochemistry.

This study says that the cause of parkinsons is due to a decrease in Tyrosine Hydroxylase activity. Interesting... I wonder if this stack would help someone with Parkinsons?

Edited by abelard lindsay, 12 August 2012 - 07:49 AM.

[hephaestus]

Tyrosine hydroyxlase is the rate limiting enzyme from tyrosine->DA and the wiki article says dopa decarboxylase is only rate limiting when supplementing dopa directly, so I'm thinking even with elevated cAMP, tyrosine hydroxylase is still probably rate limiting. It would be interesting to see how the phenylalanine->DA rate compares to tyrosine->DA with elevated cAMP.

Edited by hephaestus, 12 August 2012 - 04:08 PM.

[autocratica]

I found out today that my sleepiness on non-stack days can be largely alleviated by supplementing with l-phenylalanine. Perhaps this is related to upregulation of Tyrosine Hydroxylase?

Hmm..let's see what's new with cAMP and Tyrosine Hydroxylase.

http://www.ncbi.nlm....pubmed/22738763

Deficiency of catecholamine syntheses caused by downregulation of phosphorylation of tyrosine hydroxylase in the cerebral cortex of the senescence-accelerated mouse prone 10 strain with aging.
...
The present study demonstrated that a decline in DA and NE concentrations was observed in the cerebral cortex of SAMP10 with aging, and this decrease of catecholamine levels was caused by impairment of their synthetic pathway. These impairments are considered to be caused by downregulation of TH phosphorylation at Ser40 as a result of PKA deficiency. The present study suggests that the decline of learning and memory abilities of SAMP10 is caused by a decrease in catecholamine synthesis in the cerebral cortex with aging.
...

So these mice, who are genetically engineered to be prone to aging faster than other mice have deficient Tyrosine Hydroxylase which causes them to have a deficiency of catecholamines and thus a decline in learning and memory abilities.


http://www.ncbi.nlm....pubmed/22293035

Modulatory effects of sesamin on dopamine biosynthesis and L-DOPA-induced cytotoxicity in PC12 cells.
Zhang M, Lee HJ, Park KH, Park HJ, Choi HS, Lim SC, Lee MK.


Source
College of Pharmacy and Research Center for Bioresource and Health, Chungbuk National University, 52, Naesudong-ro, Heungduk-gu, Cheongju 361-763, Republic of Korea.


Abstract
The effects of sesamin on dopamine biosynthesis and L-DOPA-induced cytotoxicity in PC12 cells were investigated. Sesamin at concentration ranges of 20-75 μM exhibited a significant increase in intracellular dopamine levels at 24 h: 50 μM sesamin increased dopamine levels to 133% and tyrosine hydroxylase (TH) activity to 128.2% of control levels. Sesamin at 20-100 μM rapidly increased the intracellular levels of cyclic AMP (cAMP) to 158.3%-270.3% of control levels at 30 min. At 50 μM, sesamin combined with L-DOPA (50, 100 and 200 μM) further increased the intracellular dopamine levels for 24 h compared to L-DOPA alone. In the absence or presence of L-DOPA (100 and 200 μM), sesamin (50 μM) increased the phosphorylation of TH, cAMP-dependent protein kinase (PKA), and cAMP-response element-binding protein (CREB), as well as the mRNA levels of TH and CREB for 24 h, an effect which was reduced by L-DOPA (100 and 200 μM). In addition, 50 μM sesamin exhibited a protective effect against L-DOPA (100 and 200 μM)-induced cytotoxicity via the inhibition of reactive oxygen species (ROS) production and superoxide dismutase reduction, induction of extracellular signal-regulated kinase (ERK)1/2 and BadSer112 phosphorylation and Bcl-2 expression, and inhibition of cleaved-caspase-3 formation. These results suggested that sesamin enhanced dopamine biosynthesis and L-DOPA-induced increase in dopamine levels by inducing TH activity and TH gene expression, which was mediated by cAMP-PKA-CREB systems. Sesamin also protected against L-DOPA (100-200 μM)-induced cytotoxicity through the suppression of ROS activity via the modulation of ERK1/2, BadSer112, Bcl-2, and caspase-3 pathways in PC12 cells. Therefore, sesamin might serve as an adjuvant phytonutrient for neurodegenerative diseases.

So Sesamin is a cAMP increaser, like forskolin and increases phosphorylation of CREB and is a brain anti-oxidant! Is Sesamin the new Forskolin? Wow!

Sesamin is a body building supplement that's been around for some time, so this should be easy to try out.

I took Sesamin for many years for it's potential weight loss properties, I am a good responder to the forskolin+artichoke stack so I will try my hand at this.

My questions begin with I know that sesamin has an effect on PPAR alpha, and delta, I know that delta is found in the brain primarily so I am wondering if this will confound anything.

[hephaestus]

Dietary sources of tyrosine

Tyrosine, which can also be synthesized in the body from phenylalanine, is found in many high-protein food products such as chicken, turkey, fish, peanuts, almonds, avocados, milk, cheese, yogurt, cottage cheese, lima beans, pumpkin seeds, sesame seeds, bananas, and soy products.

Dietary sources of phenylalanine

L-phenylalanine is found in most foods that contain protein such as beef, poultry, pork, fish, milk, yogurt, eggs, cheese, soy products (including soy protein isolate, soybean flour, and tofu), and certain nuts and seeds. The artificial sweetener aspartame is also high in phenylalanine.

Going to try getting some more dietary tyrosine and phenylalanine and supplementing less.

Edited by hephaestus, 12 August 2012 - 06:49 PM.

[hephaestus]

Anyone supplementing SAM or TMG? I take them occasionally but not regularly. I don't know a whole lot about the methylation process other than it is involved in deactivating the catecholamines. Shouldn't I be trying to hold onto those?

Catechol-O-methyl transferase

[canz]

So I've read this thread from start to finish and have a few questions:
In regards to forskolin:

1) According to the rat study in regards to c. forksilli creating hepatoxicity in mice, the extract was 5%. Alebard lindsay has been taking the Solaray 1% extract, but have yet to see any concerns from him about hepatoxicity. Alebard if you could chime in on this: Have you had your liver values checked since dosing ~4-10mg of the forskolin at 1%?

2) Those of you taking 10-20mg of the forskolin, have you figured out what alleviates the tiredness that builds over time? Is it choline, is it glutamine, or just 1-2 days off every week or every other week?

3) Those of you taking 10-20mg of the forskolin, have you notice physical benefits (decreased body fat/increased muscle mass)? I read that zbarnes enjoyed the physical benefits at 20mg, was curious if anyone else (Health Nutty) has noticed this?

I have anxiety/depression/brain fog that comes and goes, and this stack sounds promising, but funds are tight so before I can commit to buying this stuff I just need to clarify some things. I also beleive in the minimum effective dose so I want to be able to take the lowest dose possible to reap the benefits without horrendous side effects (especially the anxiety and irritability...I have enough of that to begin with).

I'm also looking at this stack in way of physical benefit. I could use some assistance in decrease of bodyfat and increase of lean muscle so I'm willing to dose forskolin at 10-20mg in order to see the mental and physical benefits. I just need to figure out what you all have found that alleviates the burnout/tiredness that comes about from this high of a dose.

Does anyone have any feedback on the above?

[Major Legend]

Thanks abe thats really great stuff

I doubt anything were doing is that dangerous phenylalanine and tyrosine have enough negative feedback to keep dopamine in check i think i would be surprised if anyone can cause extreme excess dopamine by just taking those two.

Even with COMT inhibition i doubt the change in dopamine levels will be dangerous at least in the short term. First of all it seems a much more natural form of augmentation. I mean amphetamines work on a much more dangerous mechanism in my opinion and so do irreversible mao inhibitors.

Also dosages are famously finicky with parkinson patients, most literally take way too much thus resulting in the on and off cycle that the patients end up with. With the amount of sinemet and levodopa these patients are taking thus mao bs or even dopamine agonists this puts the surge way beyond what we would use for therapuetical purposes anyways unless were really stupid.

As you say its confounded by the disease so its hard to tell, but i reckon even in severe cases of parkinsons tardive dyskenesia the patients mind seems sound in comparison, so peripheral side effects would come first. If it was causing brain damage on the level of say methamphetamine does then i reckon people would notice.

Of course i think people should still be careful and this common theme of excess dopamine leading to apotosis is worrying indeed, these processes could go on for years without thr users noticing any problems, i am hoping that this is heavily dose reliant and it doesnt happen often.


Thanks abe thats really great stuff

I doubt anything were doing is that dangerous phenylalanine and tyrosine have enough negative feedback to keep dopamine in check i think i would be surprised if anyone can cause extreme excess dopamine by just taking those two.

Even with COMT inhibition i doubt the change in dopamine levels will be dangerous at least in the short term. First of all it seems a much more natural form of augmentation. I mean amphetamines work on a much more dangerous mechanism in my opinion and so do irreversible mao inhibitors.

Also dosages are famously finicky with parkinson patients, most literally take way too much thus resulting in the on and off cycle that the patients end up with. With the amount of sinemet and levodopa these patients are taking thus mao bs or even dopamine agonists this puts the surge way beyond what we would use for therapuetical purposes anyways unless were really stupid.

As you say its confounded by the disease so its hard to tell, but i reckon even in severe cases of parkinsons tardive dyskenesia the patients mind seems sound in comparison, so peripheral side effects would come first. If it was causing brain damage on the level of say methamphetamine does then i reckon people would notice.

Of course i think people should still be careful and this common theme of excess dopamine leading to apotosis is worrying indeed, these processes could go on for years without thr users noticing any problems, i am hoping that this is heavily dose reliant and it doesnt happen often.


Sorry ipad ^

[gizmobrain]

So I've read this thread from start to finish and have a few questions:
In regards to forskolin:

1) According to the rat study in regards to c. forksilli creating hepatoxicity in mice, the extract was 5%. Alebard lindsay has been taking the Solaray 1% extract, but have yet to see any concerns from him about hepatoxicity. Alebard if you could chime in on this: Have you had your liver values checked since dosing ~4-10mg of the forskolin at 1%?

2) Those of you taking 10-20mg of the forskolin, have you figured out what alleviates the tiredness that builds over time? Is it choline, is it glutamine, or just 1-2 days off every week or every other week?

3) Those of you taking 10-20mg of the forskolin, have you notice physical benefits (decreased body fat/increased muscle mass)? I read that zbarnes enjoyed the physical benefits at 20mg, was curious if anyone else (Health Nutty) has noticed this?

I have anxiety/depression/brain fog that comes and goes, and this stack sounds promising, but funds are tight so before I can commit to buying this stuff I just need to clarify some things. I also beleive in the minimum effective dose so I want to be able to take the lowest dose possible to reap the benefits without horrendous side effects (especially the anxiety and irritability...I have enough of that to begin with).

I'm also looking at this stack in way of physical benefit. I could use some assistance in decrease of bodyfat and increase of lean muscle so I'm willing to dose forskolin at 10-20mg in order to see the mental and physical benefits. I just need to figure out what you all have found that alleviates the burnout/tiredness that comes about from this high of a dose.

• My liver enzymes were in range on the last test.
• My sleep schedule is erratic right now, so I don't know how much tiredness is caused from the stack and how much is from my work. I usually take breaks from the forskolin about 2 days a week and I have found Galantamine, sublingual uridine, modafinil, and 1-2g doses of l-phenylalanine all to help with tiredness. Obviously, don't take these all at once!
• I work a physically demanding job. When I started taking forskolin, I noticed leaner muscle mass. Since the job has stayed consistently hard, but not any harder, my muscles haven't gotten any bigger.

If you live in the US, PM me if you want a cheap bottle of forskolin. I could send you a few days trial of the other stuff too (I have a big bottle of Quercetin and L-Phenylalanine), if you wanted to try it without having to commit to buying a whole bunch of everything.

Edited by zrbarnes, 13 August 2012 - 05:39 PM.

[health_nutty]

So Sesamin is a cAMP increaser, like forskolin and increases phosphorylation of CREB and is a brain anti-oxidant! Is Sesamin the new Forskolin? Wow!

Sesamin is a body building supplement that's been around for some time, so this should be easy to try out.

Do we have any reason to believe this will be superior to forskolin for LTP? Is it just the additional benefit of being a brain anti-oxidant?

If you try this out, let me know how it works for you.

[gizmobrain]

So Sesamin is a cAMP increaser, like forskolin and increases phosphorylation of CREB and is a brain anti-oxidant! Is Sesamin the new Forskolin? Wow!

Sesamin is a body building supplement that's been around for some time, so this should be easy to try out.

Do we have any reason to believe this will be superior to forskolin for LTP? Is it just the additional benefit of being a brain anti-oxidant?

If you try this out, let me know how it works for you.

I am planning on ordering some Scivation brand Sesamin tomorrow.

I haven't gotten any interest in a group buy of the 98% forskolin, so I figure I'll try this out in the meantime.

Edited by zrbarnes, 13 August 2012 - 05:57 PM.

[health_nutty]

So Sesamin is a cAMP increaser, like forskolin and increases phosphorylation of CREB and is a brain anti-oxidant! Is Sesamin the new Forskolin? Wow!

Sesamin is a body building supplement that's been around for some time, so this should be easy to try out.

Do we have any reason to believe this will be superior to forskolin for LTP? Is it just the additional benefit of being a brain anti-oxidant?

If you try this out, let me know how it works for you.

I am planning on ordering some Scivation brand Sesamin tomorrow.

I haven't gotten any interest in a group buy of the 98% forskolin, so I figure I'll try this out in the meantime.

Great!

[canz]

So I've read this thread from start to finish and have a few questions:
In regards to forskolin:

1) According to the rat study in regards to c. forksilli creating hepatoxicity in mice, the extract was 5%. Alebard lindsay has been taking the Solaray 1% extract, but have yet to see any concerns from him about hepatoxicity. Alebard if you could chime in on this: Have you had your liver values checked since dosing ~4-10mg of the forskolin at 1%?

2) Those of you taking 10-20mg of the forskolin, have you figured out what alleviates the tiredness that builds over time? Is it choline, is it glutamine, or just 1-2 days off every week or every other week?

3) Those of you taking 10-20mg of the forskolin, have you notice physical benefits (decreased body fat/increased muscle mass)? I read that zbarnes enjoyed the physical benefits at 20mg, was curious if anyone else (Health Nutty) has noticed this?

I have anxiety/depression/brain fog that comes and goes, and this stack sounds promising, but funds are tight so before I can commit to buying this stuff I just need to clarify some things. I also beleive in the minimum effective dose so I want to be able to take the lowest dose possible to reap the benefits without horrendous side effects (especially the anxiety and irritability...I have enough of that to begin with).

I'm also looking at this stack in way of physical benefit. I could use some assistance in decrease of bodyfat and increase of lean muscle so I'm willing to dose forskolin at 10-20mg in order to see the mental and physical benefits. I just need to figure out what you all have found that alleviates the burnout/tiredness that comes about from this high of a dose.

• My liver enzymes were in range on the last test.
• My sleep schedule is erratic right now, so I don't know how much tiredness is caused from the stack and how much is from my work. I usually take breaks from the forskolin about 2 days a week and I have found Galantamine, sublingual uridine, modafinil, and 1-2g doses of l-phenylalanine all to help with tiredness. Obviously, don't take these all at once!
• I work a physically demanding job. When I started taking forskolin, I noticed leaner muscle mass. Since the job has stayed consistently hard, but not any harder, my muscles haven't gotten any bigger.

If you live in the US, PM me if you want a cheap bottle of forskolin. I could send you a few days trial of the other stuff too (I have a big bottle of Quercetin and L-Phenylalanine), if you wanted to try it without having to commit to buying a whole bunch of everything.

Thanks for your feedback. I have phenylalanine, and wasn't interested in quercetin part of this stack. I am looking into the sesamin now as well. Thank you for your offer, if I decide I am going this route I'll PM you soon.

[health_nutty]

[
3) Those of you taking 10-20mg of the forskolin, have you notice physical benefits (decreased body fat/increased muscle mass)? I read that zbarnes enjoyed the physical benefits at 20mg, was curious if anyone else (Health Nutty) has noticed this?

I missed this in the thread. I have gotten a lot leaner since taking this stack (and I was already fairly lean). I'm actually getting a six pack for the first time (at age 36). I've always been naturally very lean (skinny), but for some reason I never had low enough bf for a six pack. I can't say for sure that it is the forskolin as I haven't tightly controlled all the other variables.

[unbeatableking]

I can attest that this stack does indeed work.

Brings my memory back to baseline levels after extended hours of staying awake. No perceptible negatives to it either.

Definitely goes well in hand with Piracetam. There is a sense of consistency to my regimen now.

[unbeatableking]

For those of you who have plans of taking the stack with Piracetam, I advise taking Piracetam 30 minutes after CILTEP.

Gorge on water. Copious amounts of water.

I have gotten the best results that way.

[RS3RS]

Dietary sources of tyrosine

Tyrosine, which can also be synthesized in the body from phenylalanine, is found in many high-protein food products such as chicken, turkey, fish, peanuts, almonds, avocados, milk, cheese, yogurt, cottage cheese, lima beans, pumpkin seeds, sesame seeds, bananas, and soy products.

Dietary sources of phenylalanine

L-phenylalanine is found in most foods that contain protein such as beef, poultry, pork, fish, milk, yogurt, eggs, cheese, soy products (including soy protein isolate, soybean flour, and tofu), and certain nuts and seeds. The artificial sweetener aspartame is also high in phenylalanine.

Going to try getting some more dietary tyrosine and phenylalanine and supplementing less.

Don't both of these substances compete for absorbtion with amino acids? I always thought you should take either of them by themselves on an empty stomach, otherwise you won't experience the same benefits. My anecdotal experience reflects that theory as well.

[hephaestus]

They are both amino acids, so they compete with other amino acids for transport. You will get the quickest effects by taking them on an empty stomach, but you will still absorb them even if you have eaten a bunch of protein, just more slowly.

[Major Legend]

On a side note I feel Quercetin is too strong for the purposes of CILTEP, plus the long half life. I've been experiencing some rebound effects with it, I think I react sensitively to most things so its probably a non issue with most. On the other hand no issues with Artichoke extract, it seems a lot more benign to me.

[victortsoi]

This may have been discussed earlier in the thread, but I'm really wondering if long term racetam/choline use may initially downregulate neurotransmitters responsible for memory, leading to a long term rebound effect where cessation promotes higher density of those same neurotransmitters/receptors. Or do we just return to baseline....(that would suck :\)

[brainslugged]

Well, CILTEP definitely increases my ability to respond to stimulants. Caffeine makes me even more irritable than before (with just the racetams, it makes me feel a bit irritable, and with no nootropics, it has no effect). I also seem to respond to L-tyrosine now, which I did not respond to before in any way other than as mild negative physical symptoms. I still do not notice any difference in memory, but there is definitely still a difference in working memory, and I think one in concentration. I am going to up the doses soon and see what happens. More tyrosine action would actually be my preferred result. It is amazing what a small increase in dopamine does for your thinking.

[owtsgmi]

On a side note I feel Quercetin is too strong for the purposes of CILTEP, plus the long half life. I've been experiencing some rebound effects with it, I think I react sensitively to most things so its probably a non issue with most. On the other hand no issues with Artichoke extract, it seems a lot more benign to me.

Could you elaborate (tiredness, hyper-viligence, by chance)?

Edited by owtsgmi, 15 August 2012 - 05:13 AM.

[unbeatableking]

How does the stack fare without forskolin? Ran out of it and will be getting my supply tomorrow.

I have a study session tonight and all I have on hand are Piracetam and Quercetin.