So, once again Steve was kind enough to do an IC special and as a result I've got 25 grams of L-Dopa to try.

I mainly wanted to try it because I've used USP Labs 1-Carboxy with success and saw the threads debating whether they were essentially the same thing.

I haven't taken 1-Carboxy for around two months probably but still have some so I figure I'll run the L-Dopa for ~ 2 weeks and compare it to my first experiences with 1-Carboxy. Then take a couple weeks off and try the 1-Carboxy again to be sure I still notice the same effects from it.

I'm primarily trying to see if I notice the sleep effects that I noticed on 1-Carboxy so I will be taking it ~ 45 min before bed. Dosage will be 1 gram, at least starting out. Any input on dosing, or anything else for that matter, is certainly welcome.

I didn't feel any effect at up to about 1 gram, after which I began to feel "burnt out" with no pleasant experience to justify the washout period (which isn't surprising considering L-Dopa's half-life is only about an hour or so).

I would suggest starting out at 250-500 mg and ideally taking it with green tea.

Does this apply to someone on Deprenyl/Selegiline as well or would you suggest a lower dose?

Thanks for teh recs, Steve. I'll look into that further when I get a chance Dopamine.

First night I took 1 gram. The second night I took 500 mg and will continue at that dose; couldn't tell a difference anyway. Yeah, took GTE with it.

Both times I felt quite groggy when it was time to lay down to bed, but it took a little bit to fall asleep. My mind kept racing. My mind does that a lot at night though. Plus, with a couple of things going on, it's probably heightend. I also tossed around trying to find a comfortable position moreso than usual. Also, I normally wake up at least two times during the night but can usually go right back to sleep when I try to. It took about 15-20 minutes both nights though. Could be a coincidence though. I'll keep an eye on it.

L-Dopa: Growth hormone releaser

If L-dopa were useful only as a PD treatment, it would be of little interest to most people. Yet L-dopa has uses beyond PD. It has been known for over 30 years that it is an effective stimulant of human growth hormone (HGH) release. In 1970, Boyd and colleagues found that a 500mg oral dose …"caused a significant rise in plasma growth hormone in PD patients, initially starting therapy or on chronic L-dopa therapy for as long as 11 months. The rise in plasma growth hormone persisted for 120 minutes after the administration of the drug." (4). Boden and his co-workers gave 500mg of the drug orally to four male and five female volunteers. "HGH levels rose sharply at 45 minutes from the basal value of 0.8mg/ml, to a maximum of 10.0mg/ml at 90 minutes (p<0.001) and declined thereafter. This rise occurred in eight of the nine subjects." (5). Hayek and Crawford reported that six out of seven "constitutionally short children" responded to oral L-dopa (200-500mg), "…with elevations in HGH concentration above 7mg/ml, peak levels occurring between 30 and 120 minutes after drug administration..". (6).

In 1975, Ajlouni and colleagues reported the effects of 500mg of oral L-dopa on eight normal and 8 non-obese insulin-dependent diabetic subjects. The normal subjects increased their plasma HGH from 1.5mg/ml before L-dopa, to an average 21mg/ml at 90 minutes post L-dopa, with all subjects showing at least a 10 mg/ml increase. The diabetics increased from 2.5mg/ml to 20mg/ml from 60-90 minutes post L-dopa. Giving 100 grams (3 _ ounces) of glucose with, or 30 minutes after the drug totally suppressed the expected HGH increase (7).

Obesity has been shown to blunt HGH release after oral L-dopa. Laurian and his co-workers tested 17 obese, non-diabetic and six normal weight volunteers. All 17 obese subjects failed to respond to L-dopa, while the normal weight subjects had HGH increases of 10-11mg/ml at 90 and 120 minutes after the drug was administered. The 17 obese men and women subsequently lost 12-50kg. After weight loss, 8 people secreted HGH in response to L-dopa, but at levels only 50-60% of the normal weight people. 9 formerly obese people still failed to respond to it (8).

Barbarino and colleagues gave 500mg orally to 12 obese people, with no significant HGH increases. When some of the subjects were given 40mg oral Propranolol, two hours before L-dopa, they then showed HGH response, although at only 50-75% of the level shown by 12 normal weight subjects given L-dopa, whose serum HGH levels reached 7 to 32mg/ml 60-120 minutes after L-dopa (9).

Greenspan et al. compared HGH response to L-dopa in 44 young patients (31-44 years of age) and 42 older patients (64-88 years of age). All were considered "healthy participants". Plasma HGH increased by 221% in the young patients and 167% in the older patients. The post L-dopa HGH levels were similar in young and old (4.5 and 4.8mg/ml) (10).

The preceding studies illustrate some of the studies showing that 500mg oral L-dopa is an effective stimulator of HGH release. Whether a person is male or female, young or old, diabetic or not, thin or obese (possibly with Propranolol), a PD patient or not, L-dopa is a natural HGH-releasing agent when taken on an empty stomach. For those who can't afford HGH injections, or just don't like self-injecting,L-dopa may provide a reasonable alternative.


L-DOPA Enhances Memory in Healthy Adults

Ann Neurol. 2005 Jul;58(1):121-30
Dopaminergic influences on formation of a motor memory.

Floel A, Breitenstein C, Hummel F, Celnik P, Gingert C, Sawaki L, Knecht S, Cohen LG. Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20817, USA.

The ability of the central nervous system to form motor memories, a process contributing to motor learning and skill acquisition, decreases with age. Dopaminergic activity, one of the mechanisms implicated in memory formation, experiences a similar decline with aging. It is possible that restoring dopaminergic function in elderly adults could lead to improved formation of motor memories with training. We studied the influence of a single oral dose of levodopa (100mg) administered preceding training on the ability to encode an elementary motor memory in the primary motor cortex of elderly and young healthy volunteers in a randomized, double-blind, placebo-controlled design. Attention to the task and motor training kinematics were comparable across age groups and sessions. In young subjects, encoding a motor memory under placebo was more prominent than in older subjects, and the encoding process was accelerated by intake of levodopa. In the elderly group, diminished motor memory encoding under placebo was enhanced by intake of levodopa to levels present in younger subjects. Therefore, upregulation of dopaminergic activity accelerated memory formation in young subjects and restored the ability to form a motor memory in elderly subjects; possible mechanisms underlying the beneficial effects of dopaminergic agents on motor learning in neurorehabilitation.

Ann Neurol. 2004 Jul;56(1):20-6
Levodopa: faster and better word learning in normal humans.

Knecht S, Breitenstein C, Bushuven S, Wailke S, Kamping S, Floel A, Zwitserlood P, Ringelstein EB. Department of Neurology, University of Munster, Albert-Schweitzer-Strasse 33, D-48129 Munster, Germany. knecht@uni-muenster.de

Dopamine is a potent modulator of learning and has been implicated in the encoding of stimulus salience. Repetition, however, as required for the acquisition and reacquisition of sensorimotor or cognitive skills (e.g., in aphasia therapy), decreases salience. We here tested whether increasing brain levels of dopamine during repetitive training improves learning success. Forty healthy humans took 100mg of the dopamine precursor levodopa or placebo daily for 5 days in a randomized double-blind and parallel-group design. Ninety minutes later on each day, subjects were trained on an artificial vocabulary using a high-frequency repetitive approach. Levodopa significantly enhanced the speed, overall success, and long-term retention of novel word learning in a dose-dependent manner. These findings indicate new ways to potentiate learning in a variety of domains if conventional training alone fails.

Mol Pharmacol. 2006 Mar;69(3):968-74. Epub 2005 Nov 29.

Increased divalent metal transporter 1 expression might be associated with the neurotoxicity of L-DOPA.

Chang YZ, Ke Y, Du JR, Halpern GM, Ho KP, Zhu L, Gu XS, Xu YJ, Wang Q, Li LZ, Wang CY, Qian ZM.

Department of Applied Biology and Chemistry Technology, The Hong Kong Polytechnic University, Kowloon, Hong Kong.

Based on the available data, we speculated that changes in brain iron metabolism induced by L-DOPA might be associated with the neurotoxicity of L-DOPA. To investigate this possibility, the effects of L-DOPA on the expression of iron influx proteins [transferrin receptor (TfR) and divalent metal transporter 1 (DMT1)], iron efflux protein (ferroportin 1), and iron uptake in C6 glioma cells were determined in this study using Northern blot and Western blot analysis and the calcein method. The findings showed that treatment of C6 cells with different concentrations of L-DOPA (0-100 microM) did not affect the expression of mRNA and protein of TfR and DMT1 with iron-responsive element (+IRE) and protein of ferroportin 1. However, a significant increase in the expression of DMT1(-IRE) mRNA and protein was found in cells treated, respectively, with 10 and 30 microM L-DOPA (mRNA) and 1, 5, 10 and 30 microM L-DOPA (protein). The increase in DMT(-IRE) protein induced by L-DOPA treatment was in parallel with the increase in DMT(-IRE) mRNA. The levels of DMT1(-IRE) mRNA and protein peaked in the cells treated with 10 microM L-DOPA and then decreased progressively with increasing concentrations of L-DOPA. Further study demonstrated that treatment of the cells with 10 microM L-DOPA induced a significant increase in ferrous uptake by C6 glioma cells. The findings suggested that the increased DMT1(-IRE) expression might be partly associated with the neurotoxicity of L-DOPA. Clinical relevance of the findings needs to be investigated further.

Brain Res. 2005 Nov 30;1063(2):180-6. Epub 2005 Oct 28.

l-DOPA administration enhances 6-hydroxydopamine generation.

Maharaj H, Sukhdev Maharaj D, Scheepers M, Mokokong R, Daya S.

Division of Pharmacology, Faculty of Pharmacy, Rhodes University, P.O. Box 94, Grahamstown, 6139, South Africa.

The therapeutic success of L-3,4-dihydroxyphenylalanine (L-DOPA) treatment in Parkinson's disease (PD) patients remains controversial as many patients become tolerant requiring higher dosage regimens. However, the increase in dosage regimens results in the patients experiencing intolerable side effects. This study sought to investigate whether dopamine (DA) can chemically react with iron to form the potent neurotoxin 6-hydroxydopamine (6-OHDA). Furthermore, rats were treated with L-DOPA for a period of 7 and 28 days to determine whether L-DOPA treatment results in 6-OHDA formation in rat striatum. In addition, this study also investigates the complex interactions of L-DOPA with iron by performing in vitro and in vivo lipid peroxidation studies and the detection of endogenous 6-OHDA in iron-infused rats. In each study, melatonin was used to determine whether it could quench any free radical effects that may occur. The results of the present study show that DA chemically reacts with iron to form 6-OHDA. Moreover, L-DOPA treatment results in endogenous 6-OHDA formation in rat brain as well as enhances iron-induced lipid peroxidation both in vitro and in vivo in the rat striatum. The L-DOPA-induced increase in lipid peroxidation, in iron-infused rats, corresponds with an increase in levels of 6-OHDA in the rat striatum. The use of melatonin significantly decreases the L-DOPA-stimulated 6-OHDA formation in the rat striatum. The present study provides novel information on L-DOPA-induced neurotoxicity and suggests the concomitant use of an antioxidant with L-DOPA in order to enhance the life span of L-DOPA therapy.

PMID: 16257392

I take my in the morning or prior to working out.

I'm curious why you're taking it at night since its non ideal to have high dopamine levels at night.

There was a thread on AM where PA was saying that L-Dopa = 1-Carboxy. I know Marc said he noticed totally different results from the two, and I've used 1-Carboxy so was wanting to compare them. Since I took the 1-carboxy pre-bed, I figured I'd take L-dopa pre-bed as well.

If you think it'd be better served taken morning, I'll switch it up though.

Just to let people know. I'm not bailing on this. I've been sick for the better part of a week and haven't been taking it since.

Thanks for the well wishes!

Update:

Haven't taken it since getting better. Dr. thought I might have had appendicitis, but luckily it wasn't and I'm better. I'm out of town right now on business and will start taking it again next week when I get back. Thinking I'll switch it up to morning dosing because it didn't have an effect on sleep quality like 1-carboxy did. If anything my mind was racing with thoughts when laying in bed more than usual; which is a lot anyways.

Today marks two weeks that I've been on it straight except for Sunday and Monday of last week because I was sick. I think I had food poisoning. Don't know what I was thinking getting raw oysters at Spondivits (Kim might recall).

Anyway...since I've been on, I've had a greater sense of well-being and have been much more optimistic about day to day life. This in turn has enabled me to concentrate better at work and not get so restless and frustrated. I'm usually always focusing on any little thing that I don't like about myself/life, but not so much the last couple of weeks. Nothing in my life has changed so there is no reason for it like meeting a new woman or anything.

Definitely gets a good review from me. One possible thing...the last few nights I have had a little more trouble falling asleep but no trouble staying asleep. Not sure if it's related or not though as the first 8-10 days I had no more trouble than usual falling asleep.

I'll be cycling off and probably start taking it more as needed in the future. Oh, the dosing that I did was ~ 500mg a little after taking my green tea cap in the morning.

Nah, didn't cycle. Did it daily except the two days mentioned. I'll be off it at least 2 weeks and then use it just on an as-needed basis from here on out. Thanks again.

That quote makes sense. Thanks for posting it.