I found this to be an excellent supplement for myself, which overcomes the rate limiting step when the body converts tryptophan to 5-HTP. I am sleeping much better and handling life's normal stresses better. If you haven't already, become familiar with how/why the body converts L-Tryptophan > 5-HTP > Serotonin > Melatonin. Very interesting! Thank you Bulk Nutrients for making this available.

At first, the mice showed an irregular smattering of neural impulses when they heard the baby's cries. Then, as the oxytocin kicked in, the signal evolved into a more orderly pattern typical of a maternal brain. The study showed in unusual detail how the hormone changed the behaviour of neurons1. “Oxytocin is helping to transform the brain, to make it respond to those pup calls,” Froemke says.
The group had first identified the thymosin sulfoxide as an active factor in culture fluid of cells responding to treatment with a steroid hormone, suggesting that its formation might form part of the mechanism by which steroids exert anti-inflammatory effects. Extracellular thymosin β4 would be readily oxidised to the sulfoxide in vivo at sites of inflammation, by the respiratory burst.[21]

Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons make other peptides, including corticotropin-releasing hormone and dynorphin, for example, that act locally. The magnocellular neurosecretory cells that make oxytocin are adjacent to magnocellular neurosecretory cells that make vasopressin. These are large neuroendocrine neurons which are excitable and can generate action potentials.[124]
Bromodeoxyuridine (BrdU), a thymidine analogue, can be incorporated into the DNA of dividing cells and is widely used to label new cells.61-63 To label proliferating cells, BrdU (100 mg/kg) was injected i.p. daily starting at day 1 post TBI for 10 days. The number of BrdU-positive cells found in the ipsilateral cortex, DG, and CA3 areas was significantly increased 35 days after TBI compared with sham controls.18,34,64,65 Tβ4 treatment further increased the number of BrdU-positive cells compared to saline controls.34 The increased number of BrdU-positive cells may result from effects of Tβ4 on either increasing cell proliferation or reducing cell death of newborn cells. Our recent data show Tβ4 increases oligodendrocyte precursor cell proliferation and differentiation in animal models of stroke25 and experimental autoimmune encephalomyelitis.27 Tβ4 may not directly affect cell proliferation but inhibit cell death, for example, in corneal and conjunctival epithelial cells treated with benzalkonium chloride in vitro66 and endothelial precursor cells under serum deprivation.67 Our data further show that neurogenesis increases in TBI rats treated with Tβ4, suggesting that Tβ4 promotes newborn cells to differentiate into neurons. This is consistent with the effect of Tβ4 on promoting epicardium-derived progenitor cell differentiation into endothelial and smooth muscle cells to form the coronary vasculature.22 Whether the increased number of BrdU-positive cells in the brain of TBI rats treated with Tβ4 is tissue specific remains unknown. Tβ4 may not directly affect cell proliferation. Increased cell proliferation and neurogenesis are also possibly secondary to that Tβ4-mediated angiogenesis, as described later.
An estimated 1.4 million people sustain traumatic brain injury (TBI) each year in the United States, and more than 5 million people are coping with disabilities from TBI at an annual cost of more than $56 billion.1 There are no commercially-available pharmacological treatment options available for TBI because all clinical trial strategies have failed.2,3 The disappointing clinical trial results may be due to variability in treatment approaches and heterogeneity of the population of TBI patients.4-9 Another important aspect is that most clinical trial strategies have used drugs that target a single pathophysiological mechanism, although many mechanisms are involved in secondary injury after TBI.4 Neuroprotection approaches have historically been dominated by targeting neuron-based injury mechanisms as the primary or even exclusive focus of the neuroprotective strategy.3 In the vast majority of preclinical studies, the treatment compounds are administered early and, frequently, even before TBI.10,11 Clinically, the administration of a compound early may be problematic because of the difficulty in obtaining informed consent.12
Serotonin appears to be associated with panic attacks. Although studies that have used tryptophan depletion techniques in humans do not necessarily induce a panic attack[34][35][36] it appears it may sensitize the body by an increase in neurovegetative panic symptoms and increased anxiety[37] which suggests that serotonin is protective against panic attacks, at least acutely.[38][39] A study in 24 unmedicated panic disorder patients and normal participants given 200mg 5-HTP prior to a 35% CO2 test (used to induce a panic attack-like response) noted that the test was able to induce panic attack in both panic disorder patients and normal persons and that 200mg 5-HTP was protective in both conditions but to a greater degree in persons suffering from panic disorders.[40] This has been replicated with cholecystokinin-4 induced panic attack with 200mg 5-HTP in otherwise healthy persons.[41]

Jump up ^ Xu J, Jian B, Chu R, Lu Z, Li Q, Dunlop J, Rosenzweig-Lipson S, McGonigle P, Levy RJ, Liang B (December 2002). "Serotonin mechanisms in heart valve disease II: the 5-HT2 receptor and its signaling pathway in aortic valve interstitial cells". The American Journal of Pathology. 161 (6): 2209–18. doi:10.1016/S0002-9440(10)64497-5. PMC 1850896. PMID 12466135.

I bought 200mg "double strength" tablets off Amazon. Immediately after taking them, I felt slightly better. After a week of taking one of these with my breakfast, I could easily get through a working day without being too panicked to concentrate on a screen. I still woke up with 'the fear' but it was lessened. Better yet, there seemed to be no notable side effects. I started recommending it to all my friends with mild depression or anxiety. I was in love.
Increasing trust and reducing fear. In a risky investment game, experimental subjects given nasally administered oxytocin displayed "the highest level of trust" twice as often as the control group. Subjects who were told that they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk-aversion.[18] Nasally administered oxytocin has also been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).[19] There is no conclusive evidence for access of oxytocin to the brain through intranasal administration, however.
Drug interaction: Impact on effects of alcohol and other drugs: According to several studies in animals, oxytocin inhibits the development of tolerance to various addictive drugs (opiates, cocaine, alcohol), and reduces withdrawal symptoms.[68] MDMA (ecstasy) may increase feelings of love, empathy, and connection to others by stimulating oxytocin activity primarily via activation of serotonin 5-HT1A receptors, if initial studies in animals apply to humans.[69] The anxiolytic Buspar (buspirone) may produce some of its effects via 5-HT1A receptor-induced oxytocin stimulation as well.[70][71]
There have been some side effects reported while using Melanotan 2, typically these effects appear during the first few days of dosing and will become increasingly less obvious as the body adjusts to the peptide. These effects include: nausea, appetite loss, drowsiness and increased sex drive. In order to combat nausea, an anti-histamine can be taken when injecting until the body gets used to it. But most common way to deal with this is to inject Melanotan before bed, this is also beneficial to combat any drowsiness.
First, dietary supplements are not regulated as drugs in the US, and the careful testing and quality control that are required of prescription drugs do not apply to supplements like 5-HTP. This is why serious adverse effects and major outbreaks, like the one associated with tryptophan, can occur. You can minimize this risk by using only USP-Verified supplements.

One way to clarify that question is to give individuals oxytocin rather than just measure naturally occurring levels. In experiments by couple therapist and researcher Beate Ditzen at the University of Zurich, couples each sprayed a liquid containing oxytocin up their noses (which ensures that the hormone reaches the brain). Ditzen then got them to talk with each other about an issue that both partners said often lead to disagreement or fighting, such as who did the housework or how they spent their free time. She observed how they communicated with each other during the discussion compared with couples who didn’t get the hormone.
Evidence accumulated over the past decades has overturned the traditional dogma that the adult mammalian brain cannot generate new neurons. Adult neurogenesis has been identified in all vertebrate species examined thus far including humans.44-49 Newly generated neuronal cells originate from neural stem cells in the adult brain. Neural stem cells are the self-renewing, multipotent cells that generate the neuronal and glial cells of the nervous system.50 The major function of neurogenesis in adult brain seems to replace the neurons that die regularly in certain brain areas. Granule neurons in the DG continuously die and the progenitors in the subgranular zone of the DG may proliferate at the same rate as mature neuronal death to maintain a constant DG cell number.51 Similarly, the newly proliferated cells from the subventricular zone migrate and replenish the dead olfactory bulb neurons.52 Here, we focus on DG neurogenesis which is important for spatial learning and memory. In normal adult rats, newborn neural cells migrate from the subgranular zone of the DG of the hippocampus into the granule cell layer and eventually become mature granule neurons.53 These new granule neurons extend axonal processes to their postsynaptic targets54-57 and receive synaptic input.58 TBI stimulates widespread cellular proliferation in rats and results in focal neurogenesis in the DG of the hippocampus.59,60 Some of the newly generated granule neurons integrate into the hippocampus. The integration of the injury-induced neurogenic population into the existing hippocampal circuitry coincides with the time point when cognitive recovery is observed in injured animals.44

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In persons with Panic Disorders (versus persons without as control) ingesting 200mg of 5-HTP, both groups experienced an increase in salivary cortisol within 3 hours but the persons with Panic Attacks continued to have greater increases after the 3 hour mark; this increased cortisol was independent of any percieved side-effects such as headache, fatigue, perspiration, nausea, etc.[43]
In mammals, many mysteries remain. Oxytocin is difficult to measure reliably in the brain, making it hard to know exactly where, when and how much is normally released; nor do scientists understand precisely how it works to alter behaviour. “What we need to start thinking about is the more fundamental role that oxytocin plays in the brain,” Young says. The determination to find out has been strengthened by a growing move in neuroscience to characterize circuits that are important in brain operations. “That's the level that's critical for understanding how the brain is regulating behaviour,” says Thomas Insel, director of the US National Institute of Mental Health in Bethesda, Maryland, who has studied oxytocin in voles.

Research substantiates Wiebe's anecdotal claims. Melanotan.org, a forum dedicated to the peptide that shut down in 2011, had thousands of regular posters, many of whom have since migrated to other discussion boards. In 2009, a BBC report tracking just six needle exchanges found that hundreds of individuals had visited these exchanges in order to receive syringes for Melanotan II use. A year later, the Norwegian Pharmacy Association disclosed that, in Norway alone, several thousand syringes had been distributed to individuals seeking to inject the peptide. Linn Connie Danielsen, a model and blogger, told the Norwegian newspaper Verdens Gangthat Melanotan II helps ease the stressful impact of extended winter sun deprivation. "A nice tan in the winter is good to see," she said.


Low oxytocin levels have been linked to autism and autistic spectrum disorders (e.g. Asperger syndrome) – a key element of these disorders being poor social functioning. Some scientists believe oxytocin could be used to treat these disorders. In addition, low oxytocin has been linked to depressive symptoms and it has been proposed as a treatment for depressive disorders. However, there is not enough evidence at present to support its use for any of these conditions.

For all its positivity, however, oxytocin has a dark side. Or, more accurately, it plays a more complex role in human behavior than is commonly thought. As a facilitator of bonding among those who share similar characteristics, the hormone fosters distinctions between in-group and out-group members, and sets in motion favoritism toward in-group members and prejudice against those in out-groups. Ongoing research on the hormone is a potent reminder of the complexity of biological and psychological systems.
Total RNA was extracted from cells using Trizol (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instructions. Reverse-transcription (RT)-PCR was performed using oligo deoxythymidine primer (Roche Diagnostics, Mannheim, Germany) in 20 μl volumes at 42°C for 60 min. The RT-PCR reaction was done with 1 μg of total RNA, 1 μl of 20 μM oligo dT primer, and 18 μl of reaction mixture by AccuPower RT/PCR PreMix (Bioneer, Daejeon, Korea). Then, PCR was performed in a 20 μl total mixture volume for 25 cycles at 95°C for 1 min, 55°C for 1 min, and 72°C for 1 min. Primer sequences are detailed in Table 1. PCR products were subjected to electrophoresis on 1.5% agarose gels and visualized with ethidium bromide.
I am not a doctor and nothing I say should be taken as medical advice. If it were me, I would try TB500, and to inject simply get as close to the injury site as possible. If you want to go into detail feel free to book a consult at
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Researchers often investigate the effects of hormones on behavior in laboratory experiments with student subjects. Some studies show that when you give people oxytocin they become more generous and trusting. In others that administer testosterone to men, the opposite happens. The strength of such studies is that they can demonstrate cause and effect – the behavior change only occurs in subjects receiving hormones, not in those who get a placebo. But this research has weaknesses as well: it often focuses on single hormones, ignoring their potential interactions, and behavior is measured with highly artificial tasks.
Animal studies have found high levels of both stress and oxytocin in voles that were separated from other voles. However, when the voles were given doses of oxytocin, their levels of anxiety, cardiac stress, and depression fell, suggesting that stress increases internal production of the hormone, while externally supplied doses can help reduce stress.
Cells on the surface of the skin are constantly being replaced by regeneration from below. The repair of a wound is a scaling up of this normal process, with additional complex interactions among cells, formation of new blood vessels, collagen, more extensive cell division and cell migration, as well as strict control of inflammatory cells and the cytokines they release to resolve the inflammation.
In a 2-week long clinical trial involving 25 overweight diabetic subjects given no dietary restrictions, subjects who received 5-HTP had reduced caloric, carbohydrate, and fat intake compared to placebo. Subjects who received 5-HTP also have reduced body weight, blood sugar, insulin and HbA1C levels after 2 weeks, possibly due to changes in the diet (R).
It should be noted that, anecdotally, 5-HTP is said to reduce cravings for carbohydrates in particular. The serotonergic (related to serotonin) system plays a role in macronutrient selection particular in obese persons with a craving for carbohydrates[13] and enhancing serotonergic transmission is known to reduce these cravings.[14] Beyond this, depressed serotonergic tranmission (hypothalamus) is also implicated in increased eating and reduced satiety in general.[15]
On a personal note, 5-HTP is actually one of the 1st nootropics I ever used. When I was a teenager and would go to raves me and my friends would use 5-HTP the next day because ecstasy (MDMA) diminishes the serotonin levels. Anyone with much experience with ecstasy knows that the day(s) after can be pretty hellish because the drug so depletes your feel good neurotransmitters, 5-HTP is sort of a Biohack for this.
Double immunofluorescent staining for BrdU (red, A) and NeuN (green, B) to identify newborn neurons (yellow after merge, C) in the dentate gyrus of hippocampus from rats examined 35 days after TBI. Micrographs (D) show location of DiI injection in the CA3 region (indicated by white asterisk). In the CA3 region, axons projected from granule neurons in the dentate gyrus will take up injected DiI to their cell bodies. Co-localization (merge, H) of BrdU-positive nuclei (green, F) within retrogradely DiI labeled (red, E) granule cells were examined at 35 days after TBI. Scale bar = 25 μm (C, H). Scale bar = 50 μm (D).
Thymosin is a hormone secreted from the thymus. Its primary function is to stimulate the production of T cells, which are an important part of the immune system. Thymosin also assists in the development of B cells to plasma cells to produce antibodies. The predominant form of thymosin, thymosin b4, is a member of a highly conserved family of actin monomer-sequestering proteins. b-thymosins are the primary regulators of unpolymerized actin, and are essential for maintaining the small cytoplasmic pool of free G-actin monomers required for rapid filament elongation and allowing for the flux of monomers between the thymosin-bound pool and F-actin.
5-HTP (5-Hydroxytryptophan) is a chemical by-product of the protein building block L-tryptophan. It is also produced commercially from the seeds of an African plant known as Griffonia simplicifolia 5-HTP is used for sleep disorders such as insomnia, depression, anxiety, migraine and tension-type headaches, fibromyalgia, obesity, premenstrual syndrome (PMS), premenstrual dysphoric disorder (PMDD), attention deficit-hyperactivity disorder (ADHD), seizure disorder, and Parkinson's disease..