Thursday, March 29, 2018

DLPA seems to improve my mood (my anecdotal experience) and research

Sources:
National Center for Biotechnology Information. PubChem Compound Database; CID=994, https://pubchem.ncbi.nlm.nih.gov/compound/994 (accessed Mar. 29, 2018).

INTRO
I've purchased DLPA and L-Phenylaline. Interested in what these precursors to L-Tyrosine and the the others "focus" and "mood" related drugs do. It seems they are ideally taken with Vitamin B6/B12, which I've also been taking(well at least B6 I believe I saw)...
Appears related to SATIETY(being satisfied hormones)...ironically my appetite seems pretty ravenous on it.

Theurapeutic uses of Phenylaline

Therapeutic Uses

An essential aromatic amino acid that is a precursor of MELANIN; DOPAMINEnoradrenalin (NOREPINEPHRINE), and THYROXINE.
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
/EXPTL TREATMENT/ There is no totally effective treatment for vitiligo (localised hypopigmentation). Oral or topical photochemotherapy with psoralens is generally considered to be the best available treatment, but experimental therapy includes UVA phototherapy with phenylalanine. Use of phenylalanine in oral doses of up to 100 mg/kg with UVA/sunlight led to beneficial results in more than 90% of 200 patients with vitiligo. Greatest benefit was noted in early disease, but prolonged use still induced repigmentation in long-standing cases. Repigmentation occurred mainly in areas rich in follicles. Such therapy is contra-indicated in phenylketonuria and in pregnancy. Similarly a further open study reported responses in 94 of 149 patients receiving 50 to 100 mg/kg daily of phenylalanine plus twice weekly UVA treatment. However, only 22% of responders had repigmentation in more than 60% of the affected area. Higher doses did not seem to be more effective than 50 mg/kg daily. Another group reported on 6 years of experience of treatment of vitiligo using 50 or 100 mg/kg daily of phenylalanine, with application of 10% phenylalanine gel and daily sun exposure. Although not ideal, they considered the treatment useful, especially for its ability to rapidly repigment the face. The same group performed an open study, adding topical 0.025% clobetasol propionate, and ultraviolet exposure during autumn and winter; 65.5% of patients achieved 100% repigmentation on the face.
Sweetman SC (ed), Martindale: The Complete Drug Reference. London: Pharmaceutical Press (2009), p.1960.
/Experimental Therapy/ L-Phenylalanine (Phe), is a potent releaser of the satiety hormone, cholecystokinin (CCK) and previous studies, conducted primarily in men, show that ingestion of Phe reduces energy intake. The objective of the current study was to test the effects of Phe on energy intake in overweight and obese women. Subjects (n =3 2) received three treatments (high-dose (10 g Phe), low-dose (5 g Phe and 5 g glucose) or control (10 g glucose)) 20 min before an ad libitum lunch and dinner meal in a within-subjects', counterbalanced, double-blind study. No effect of Phe was found; however, interactions with dietary restraint status were detected in post-hoc analyses.
Abstract: PubMed
Pohle-Krauza RJ, et al; Appetite 51 (1): 111-9 (2008). Available from, as of March 25, 2010:
/Experimental Therapy/ L-phenylalanine in combination with 0.025% clobetasol propionate and sunlight during sunny months or UVA lamps in winter, appears to improve evolutive vitiligo without side effects, and therefore is especially recommended on the face or for children.
Abstract: PubMed
Camacho F, Mazuecos J; J Drugs Dermatol 1 (2): 127-31 (2002). Available from, as of March 25, 2010:
... Leucine and phenylalanine balance both changed from negative to positive during parenteral nutrition. However, leucine and phenylalanine catabolism were differently affected by parenteral nutrition; the rate of leucine oxidation increased 2-fold, whereas the rate of phenylalanine hydroxylation was unchanged from basal values. Phenylalanineutilization for protein synthesis and leucine utilization for protein synthesis (based on both plasma leucine and alpha-ketoisocaproic acid enrichments) increased significantly during parenteral nutrition. The endogenous rates of release of leucine (based on plasma leucine enrichment) and phenylalanine (both reflecting proteolysis) were significantly reduced during parenteral nutrition. The endogenous rate of release of leucine (based on alpha-ketoisocaproic acid enrichment) was slightly but not significantly lower during parenteral nutrition. The substantial increase in leucine oxidation without changes in phenylalanine hydroxylation suggests a possible limitation in the phenylalanine/tyrosine supply during parenteral nutrition. In addition, these results suggest that premature infants respond to parenteral nutrition with acute increases in whole body protein synthesis as well as a probable reduction in proteolysis. /Parenteral nutrition/
Abstract: PubMed
Clark SE, et al; Pediatr Res 41 (4 Pt 1): 568-74 (1997). Available from, as of March 25, 2010:
/Experimental Therapy/ ... To determine whether combination therapy with lofepramine, L-phenylalanine, and intramuscular vitamin B-12 (the "Cari Loder regime") reduces disability in patients with multiple sclerosis ... a placebo controlled, double blind, randomized study /was/ carried out in five United Kingdom centers on outpatients with clinically definite multiple sclerosis ... Over 24 weeks all patients received vitamin B-12, 1 mg intramuscularly weekly, and either lofepramine 70 mg and L-phenylalanine 500 mg twice daily, or matching placebo tablets. Outcome was assessed using the GNDS, the Kurtzke expanded disability status scale; the Beck depression inventory, the Chalder fatigue scale, and the Gulick MS specific symptom scale ... Patients with multiple sclerosis improved by 2 GNDS points after starting vitamin B-12 injections. The addition of lofepramine and L-phenylalanineadded a further 0.6 points benefit ...[Wade DT, et al; J Neurol Neurosurg Psychiatry 73 (3): 246-9 (2002). Available from, as of March 25, 2010:] Full text: PMC1738034
Abstract: PubMed
/Experimental Therapy/ ... The inherited cardiac dearrangement seen in adolescents with hypertensive genetic predisposition can be assumed to be the pre-hypertensive changes of essential hypertension. It can be reversed by phenylalanine - a natural and essential amino-acid.
Abstract: PubMed
Zhao G, et al; Zhonghua Yi Xue Za Zhi 77 (1): 58-61 (1997). Available from, as of March 25, 2010

One of the catecholamine NEUROTRANSMITTERS in the brain. Dopamine is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
Dopamine is a Catecholamine. The chemical classification of dopamine is Catecholamines.
The following is just a compilation from the web, I am interested in DLPA both SCIENTIFICALLY proven and anecdotal evidence.

I believe its a building block of PEA if I'm not mistaken?
https://examine.com/supplements/phenylethylamine/ (PEA)



https://pubchem.ncbi.nlm.nih.gov/compound/L-phenylalanine#section=Top

So DLPA,
Phenylalanine is an essential aromatic amino acid that is a precursor of MELANIN; DOPAMINE; noradrenalin (NOREPINEPHRINE), and THYROXINE.
  • D-form seems to help pain. D form is manmade 
  • L-Phenylaline gives more energy
  • Phenylalanine is a precursor for tyrosine, the monoamine neurotransmitters dopaminenorepinephrine (noradrenaline), and epinephrine (adrenaline), and the skin pigment melanin
  • Good sources of phenylalanine are eggs, chicken, liver, beef, milk, and soybeans
    • those with low protein or bad diet/low calories/low appetite may find they lack in it..

My experience
  • increased appetite
  • increased mood
  • increased focus
  • less sensitive to stress/ work day passed by faster etc(more social with coworkers etc)
  • more social

Biosynthetic pathways for catecholamines and trace amines in the human brain[7][8][9]
The image above contains clickable links
Phenylalanine in humans may ultimately be metabolized into a range of different substances.

Thereupatic uses of DOPAMINE

Therapeutic Uses

Cardiotonic Agents
National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)
Dopamine also is used to increase cardiac output and blood pressure in advanced cardiovascular life support (ACLS) during cardiopulmonary resuscitation. Dopamine may be considered in the treatment of symptomatic bradycardia unresponsive to atropine, as a temporizing measure while awaiting availability of a pacemaker, or if pacing is ineffective. During resuscitation, dopamine therapy often is used for the management of hypotension, particularly if associated with symptomatic bradycardia or after return of spontaneous circulation. Dopaminecombined with other agents, such as dobutamine, also may be a useful option in the management of postresuscitation hypotension. If hypotension persists after filling pressure (i.e., intravascular volume) is optimized, drugs with combined inotropic and vasopressor actions (e.g., epinephrinenorepinephrine) may be used. Some evidence from animal studies suggests that epinephrine may be more effective than dopamine in improving hemodynamics during cardiopulmonary resuscitation. In addition, epinephrine generally is preferred for patients with severe bradycardia and associated hypotension since pulseless electrical activity or even asystole may be imminent. /Included in US product label/
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 1345
The net hemodynamic effects of dopamine make it particularly useful in the treatment of cardiogenic shock (including that associated with acute myocardial infarction) or in shock in which oliguria is refractory to other vasopressor agents. Some experts state that dopamine may be considered for the treatment of drug-induced hypovolemic shock, and often is the recommended initial agent for this use when the patient is unresponsive to fluid volume expansion and inotropic and/or vasopressor support is required. The drug can be used as an adjunct (to increase cardiac output further and maintain blood pressure) to afterload reduction with vasodilators (e.g., sodium nitroprusside) in patients with left ventricular failure following acute myocardial infarction when arterial pressure decreases precipitously during afterload reduction; for less precipitous decreases, dobutamine may be preferred but should not be used alone in severely hypotensive patients. In patients with hypotensive cardiogenic shock following acute myocardial infarction, dopamine may be used to replace norepinephrine therapy once systemic arterial pressure has increased to at least 80 mm Hg. Once arterial blood pressure has been stabilized to at least 90 mm Hg, dobutamine may be used concomitantly with dopamine in such patients in an attempt to reduce dopamine requirements. Dopamine also has been used to support cardiac output and maintain arterial pressure during intra-aortic balloon counterpulsation therapy (e.g., in patients with hypotensive cardiogenic shock following acute myocardial infarction). The use of dopamine in low cardiac output syndrome following open heart surgery has been shown to increase long-term survival. However, because dobutamine lowers peripheral resistance over a wide dosage range, is not dependent on release of endogenous catecholamines for its effects, and is cardioselective, that drug may be preferable in the period immediately following cardiopulmonary bypass surgery. /Included in US product label/
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 1345
Dopamine is used to increase cardiac output, blood pressure, and urine flow as an adjunct in the treatment of shock that persists after adequate fluid volume replacement and when systemic vascular resistance is decreased. /Included in US product label/
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 1345
Dopamine seems to improve mechanical efficiency of heart in coronary artery disease and improve immediate survival from cardiogenic shock and severe heart failure.
Theroux P et al; Hemodynamic and therapeutic effects of intravenous dopamine; Can Med Assoc J 116 (Mar 19) 645 (1977)
Six cases of toxic ingestion of clonidine hydrochloride are reviewed. Hypotension was managed by volume expansion, and if necessary, by a continuous infusion of dopamine.
Olsson JM, Pruitt AW; Management of clonidine ingestion in children; J Pediatr 103(4) 646 (1983)
Massive overdosage of adrenergic drugs is assoc with severe morbidity and high mortality rate. Good clinical response was obtained following inordinately large doses of isoproterenol and dopamine together with glucagon.
Lewis M et al; Survival following massive overdose of adrenergic blocking agents (acebutolol and labetalol); Eur Heart J 4(5) 328 (1983)
Exptl use: dopamine is a novel antitumor agent that has shown activity against B16 melanoma. Four patients with advanced malignant melanoma were infused with dopamine at 20 ug/kg/min for 48-120 hr. Tumor and bone marrow samples were obtained before and after treatment for comparison. Each of patients tested showed significant reduction in labeling index of tumor cells following treatment. These results suggest that dopamine is capable of attaining cytotoxic levels necessary to induce a biochemical inhibition of human malignant melanoma.
Wick MM; Therapeutic effect of dopamine infusion on human malignant melanoma; Cancer Treat Rep 66(8) 1657 (1982)
A number of drugs have been tested for their ability to protect the lung against hyperoxia-induced injury ... Dopamine ... /shows/ protective actions against hyperoxia-induced injury.
Leikauf GD, Prows DR; Patty's Toxicology CD-ROM (2005). NY, NY: John Wiley & Sons; Inorganic Compounds of Carbon, Nitrogen, and Oxygen. Online Posting Date: April 16, 2001.
Dopamine may improve cardiac output and stroke volume and is considered useful in the short-term management of patients with severe congestive heart failure that is refractory to cardiac glycosides (digoxin) and diuretics. The relative value and role of dopamine and dobutamine in patients with congestive heart failure remain to be clearly established; however, dobutamine may be preferable to dopamine since dopamine depends for part of its action on release of endogenous catecholamines which may be depleted in patients with chronic congestive heart failure. In a limited number of studies in patients with congestive heart failure, dopamine has been used concurrently with cardiac afterload-reducing agents such as sodium nitroprusside. In patients with congestive heart failure, cardiac output increased more with concurrent use of these drugs than with either drug alone. /Included in US product label/
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 1345
Dopamine has been used as part of a regimen for treatment of hepatorenal syndrome, cirrhosis, and barbiturate, meprobamate, or salicylate intoxication; however, long-term beneficial effects have not been demonstrated. /Use not currently included in US product label/
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 1345
Although data from studies in animals and some clinical studies in a limited number of healthy or critically ill adults indicate that low-dose ... infusions of dopamine may increase renal and mesenteric perfusion as a result of selective stimulation of renal dopaminergic receptors and subsequent renal vasodilation, many clinicians currently suggest that low-dose ("renal dose") dopamine therapy does not prevent or ameliorate acute renal failure in critically ill patients. In a randomized, double-blind, placebo-controlled study, adults in an intensive care unit (ICU) at risk for acute renal failure who received dopamine as a continuous, low-dose (2 mcg/kg per minute) infusion had similar peak serum creatinine concentrations during treatment, similar durations of ICU and hospital stay, and similar survival to ICU or hospital discharge compared with those receiving placebo. Other studies in patients at high risk for renal failure receiving low-dose dopamine infusions ... have demonstrated similar findings. In a study in a small number of hemodynamically stable, critically ill patients, infusion of dopamine ... increased creatinine clearance, diuresis, and fractional excretion of sodium; however, these beneficial effects (except for diuresis) generally diminished after 24 hours, indicating the possibility of tolerance to the effects of dopamine. In addition, alterations in clearance and metabolism in critically ill patients may result in high interindividual variability in plasma dopamineconcentrations for a given infusion rate (dosage) of the drug, making it difficult or impossible to guarantee a selective effect of the drug in this patient population. Low-dose infusions of dopamine are not without risk and may be associated with adverse effects such as suppression of respiratory drive, increased cardiac output and myocardial oxygen consumption, arrhythmias, hypokalemia, hypophosphatemia, gut ischemia, and disruption of metabolic and immunologic homeostasis. /Included in US product label/
American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 1345

Wednesday, March 23, 2016

Battling phenibut tolerance - best of the web. Taking Phenibut daily would be ideal...here's a post from a user who took it

2 Years of Daily Phenibut Use - Success

phenibut 

61 replies to this topic

#1 ericzx777

  • Registered User
  • 5 posts
  • 3 ₮
  • Location:New York
  • no
Posted 06 March 2014 - 01:49 PM

DISCLAIMER: I am not a physician or heath expert. Below is a summary of my personal experience with taking phebibut, and does not constitute medical advice that only your physician can provide. Because I have had so much success with phenibut, it does not guarantee similar results for everyone … so now you can’t sue me.


I have been suffering from debilitating anxiety my entire life. I have sought treatment diligently, have been prescribed a variety of medications, to no avail. I’ve heard of phebibut online, and decided to give it a try. My life changed entirely. After taking the first dose, my anxiety was completely gone, I was able to think more clearly, act more fluidly in social situations, and turn my life around 180 degrees. I have been taking it for over 2 years, at 2 grams per day, which may sound ridiculously insane to some, so I’d just like to shed some light on that.

Firstly, everyone warns about tolerance to phebibut, and how you should take it sparingly, lest suffer. Everyone talks about ‘tolerance’ as if you’ll need more, and more and more of the dosage to yield the same effect … like it’s an infinite loop to the point where in 3-4 years you’ll have to consume seventeen pounds of the stuff to get the same effect. Nobody talks about peak tolerance. Sure, you build tolerance to any substance, but tolerance starts to peak out at a certain threshold. For me, that threshold would be 2 grams. I’ve been taking that much for over two years. Sure I’ve built tolerance, going from .5g, to 1g, to 1.5g … but it’s leveled out at 2g, and taking any more than that, even after 2 years, would make me feel drowsy and nauseous. Likewise, doctors prescribe some medications that have tolerance (e.g. Adderall, antidepresants). These medications are MEANT to be taken continuously, without cessation, as an ongoing treatment. Skipping does is not advised, because obviously, adverse symptoms would set in. Cessation, if desired, would be achieved by tapering over the course of weeks/months, not abrupt cold-turkey. Thus, dependence is sometimes explicit in treating disorders. Now, chronic phenibut use has not been extensively studied, but directly quoting from a translated Belarusian prescription guide of phenibut** “Prolonged use helps increase mental and physical workload, improves memory, helps maintain healthy sleep cycle.” citing the dosage as multiple times daily, for periods of multiple days/weeks. If you are worried about dependence or tolerance, or just want to take it a few days on/off, then you are flirting with the potential for excruciating withdrawal symptoms, and you’d be better off not taking phenibut at all.

Am I worried about dependence? Well, to prove to myself that I can live without phebibut, I’ll tell you that I have successfully quit by tapering down over the course of a month a few weeks ago. Certainly, withdrawal set it. It was horrible, but manageable since I did a slow taper. After cutting my dose down to around .5g/day and then abstaining for a few days, my anxiety returned with a vengeance. In other words, I returned to being my anxiety-filled self. And so, I’ve proven my point. Sure, I can quit phenibut (tapering down over the course of a few weeks) … but why would I want to? So I started taking my usual 2g dose every morning, and here I am, six months later. With my anxiety under control, I have accomplished more in these past two years than I have ever in my life. I went back to college, double majoring, making the dean’s list each semester. I am no longer afraid to talk to people, or go to class … I’ve made a whole new circle of friends, and each morning I am eager to wake up and achieve more.

What about long-term safety? I’ve done massive research, and read the available small-scale clinical trials. Usually you would find some negative side effects with prolonged use of a pharmaceutical; not phenibut, instead some studies have found positive long-term cognitive benefits, consistent with the monogram.**

Financial cost? Dirt cheap. I have done extensive shopping around over the past two years and by far, and Health Supplement Wholesalers the lowest rock bottom value … $150 for a kilogram, which would last me over a year and half. I can’t even get quality phenibut at that price buying wholesale from China. HealthSupplementWholesalers [dot] com

So yes, I take phebibut every single day. Just like millions of people worldwide take pharmaceutical drugs each and every day by recommendation from their physician, or for sustained medical treatment. I am only addicted to a cure that has empowered me to reach the horizons of my potential which were previously unfathomable. For some, the idea of relying on a pill for daily functioning would be unthinkable and a sign of dreaded addiction. Yet there is no issue with being dependent, if not addicted, to McDonnald jumbo meals, diabetes-infused pop soda, tanning beds and motor vehicles (responsible for thousands of fatalities per year) among other things we idolatrize daily that may carry even greater risks. Maybe substances like phenibut can empower us, just like other innovations, if we can shift our focus from their perils to their potential. Now, my optimism does not absolve the risk of the potentially long-term hazards of chronic phenibut use. I am just merely asserting that I have weighed the benefits and hazards of those risks, and have decided that for me personally … the benefits far outweigh the risks.

So, end of rant. Since the bulk of online posts about phenibut are cold-hard failure and withdrawal experiences, I'd just figured I'd share the flip side of the coin and throw in a sucess story. And again, allow me to disclaim: I do not advocate or promote the chronic use of phenibut, everyone is different. Taking phenibut as I did may turn out to be a catastrophic disaster for you. It really depends on your personality and discipline, of which you are advised to deeply assess before self-medicating in any way. Fair warning.

** I can't post links due to newbie status, but PM me if you want the link to to source. 
  •  like x 10
  •  Agree x 2
  •  dislike x 2
  •  Dangerous, Irresponsible x 1