It turns out the love hormone oxytocin is two-faced. Oxytocin has long been known as the warm, fuzzy hormone that promotes feelings of love, social bonding and well-being. It's even being tested as an anti-anxiety drug. But new Northwestern Medicine® research shows oxytocin also can cause emotional pain, an entirely new, darker identity for the hormone.
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.
Other supplements are available which have appetite supressant and mood enhancing effects similar to 5-HTP. These type of ingredients are often included, in optimal pre-formulated dosages in fat burners. Phenylethylamine is also another ingredient with mood enhancing potential that is often found in fat burners in place of 5-HTP. 5-HTP can be found in some sleep supplements, though in Australia they are replaced by ingredients such as GABA and phenibut.
Thymosin β4 (TMSB4X, Tβ4) is the most abundant G-actin binding peptide of the cytosol and is a potent proangiogenic factor. The role of myocardin-related transcription factors (MRTF) and serum response factor (SRF) for this function was examined in experimentally induced prolonged ischemic myocardium areas of transgenic pigs ubiquitously and constitutively overexpressing Tβ4 driven by the cytomegalovirus promoter. Upon induction of a reversible loss of cardiomyocyte function which is amenable to therapeutic neovascularization, transgenic pigs did not experience a significant loss of perfusion nor myocardial function at rest or under rapid pacing. Functional vascular regeneration by induced capillary growth and maturation was found in the transgenic pigs (Hinkel et al., 2014).
I broke my neck this year at C6-C7 facets. Started taking TB-500 immediately following the accident. I don’t sit still well and was back in the gym almost immediately, simply to not go stir crazy and pump the blood anyway I could. 8 weeks later I was hitting bodyweight overhead squats for reps with the jerk, 0 pain and completely stable spine. I’m in my late 30s. I eat well, sleep well, and drink a lot of water. I doubt I would have been as well off, had I not taken the TB.
How not surprising on one level that a hormone involved in the formation of primary bonds, those that can have serious impacts on your survival, would be discerning. After all, if you had a mother who was dangerous, abusive, etc., how counter productive would it be for you to bond so tightly to her that you were all over her all the time, increasing your chances of pissing her off and killing you. And, how beneficial for you to be more bonded to a mother figure who was good to you, and provided you with nurture.
Outside the brain, oxytocin-containing cells have been identified in several diverse tissues, including in females in the corpus luteum[34][35] and the placenta;[36] in males in the testicles' interstitial cells of Leydig;[37] and in both sexes in the retina,[38] the adrenal medulla,[39] the thymus[40] and the pancreas.[41] The finding of significant amounts of this classically "neurohypophysial" hormone outside the central nervous system raises many questions regarding its possible importance in these different tissues.
There are several layers in the skin; the outer epidermis and beneath it the dermis and the subcutaneous layer. Cells in the epidermis include keratinocytes, its major cell type, that move continuously from the lower basal layer where they are formed by cell division. Other cells in the epidermis are the melanocytes that synthesize pigment and transfer it to the keratinocytes, giving our skin its color, and a wide variety of immune cells that maintain immune surveillance and secrete substances called cytokines, like interleukin 1 and 2, which are active in inflammation. The dermis contains connective tissue, mainly collagen, blood vessels, various types of immune white cells and fibroblasts.

Thymosin Beta 4 is a potent peptide that comes from a family of 16 related molecules that are localized in circulating cells and tissues within the body. These molecules also have a high conservation of sequence. TB 500 conjoins with actin and prevents actin polymerization. It is noted as being the actin-sequestering molecule within eukaryotic cells. It also boosts extracellular matrix-degrading enzyme production.

Nature has been very clever in a way. Without oxytocin, you know, babies are what they really are - I probably shouldn't say this on TV - but noisy, smelly animals that don't actually do anything useful. And, um, that's what oxytocin does. It gives them a special salience, a special beauty and allows us to bond with these defenceless little animals.
During the 2000s, the Melanotan II peptide and the metabolite derived from it, the erectile dysfunction-focused Bremelanotide (also known as PT-141), were patented and then licensed to biotechnology companies hoping to develop them into profitable prescription drugs. However, these companies also offer the peptides for direct sale to researchers. These transactions occupy a legal gray area, since the peptides are banned for human use outside clinical trials. While they can be purchased from various websites specializing in research chemicals, the purchaser usually has to affirm prior to final sale that the peptide "will not be used for human consumption" and is being acquired for "research purposes only."
Don’t take it by itself, you want to take it with a meal. The half life seems to vary; some people just need to take a single dose daily whereas some break it up into several doses. The dosage range is pretty wide, from 50 to 900 milligrams. Many report the antidepressant effect desired from lower doses, so start low with this one. Do not use a liquid form of 5-HTP.
To investigate the effect of Tβ4 peptide on H2O2-induced signaling cascades, the activation states of three mitogen-activated protein kinases (MAPKs; p38, c-Jun N-terminal kinase [JNK] and extracellular signal-related kinase [ERK]) as well as NF-κB p65 were examined in PDLCs. H2O2 treatment induced the phosphorylation of p38, ERK, and JNK MAPK(s) and the nuclear translocation of NF-κB p65 (Fig 5A). Treatment of cells with Tβ4 peptide blocked H2O2-induced nuclear translocation of NF-κB p65 and phosphorylation of ERK and JNK (Fig 5B).
Disclaimer: Thymosin Beta 4 is a peptide that should only be purchased for use in experimentation and research. It should not be purchased for human use or any other purpose than for research. It is advised that once purchased, the peptide is used within experimental circumstances that are under strict lab regulations. It is recommended that researchers use protective gear in order to prevent contact with the substance. However, if exposure is made with the peptide, it is very important to cleanse the area immediately to prevent harm.

Nolen, W. A., van de Putte, J. J., Dijken, W. A., Kamp, J. S., Blansjaar, B. A., Kramer, H. J., and Haffmans, J. Treatment strategy in depression. II. MAO inhibitors in depression resistant to cyclic antidepressants: two controlled crossover studies with tranylcypromine versus L-5-hydroxytryptophan and nomifensine. Acta Psychiatr.Scand 1988;78(6):676-683. View abstract.
Delayed Tβ4 treatment increases vascular density in the injured cortex, ipsilateral dentate gyrus, and CA3 region 35 days after TBI. Arrows show vWF-stained vascular structure. TBI alone (B) significantly increases the vascular density in the injured cortex compared to sham controls (A, P < 0.05). Tβ4 treatment (C) further enhances angiogenesis after TBI compared to the saline-treated groups (P < 0.05). The density of vWF-stained vasculature in different regions is shown in (D). Scale bar = 25 μm (C). Data represent mean + SD. *P < 0.05 vs Sham group. #P < 0.05 vs Saline group. N (rats/group) = 6 (Sham); 9 (Saline); and 10 (Tβ4).

The pore-forming subunit of the cardiac sodium channel Nav1.5 encoded by SCN5A is a critical determinant of myocardial excitability and conduction. Loss-of-function mutations in SCN5A can clinically manifest as progressive cardiac conduction disorders or as arrhythmic syndromes, such as Brugada syndrome. In addition to electrophysiological dysfunction, SCN5A mutations are also associated with myocardial fibrosis manifesting as global cardiomyopathy. In a 10-year old child exhibiting Brugada syndrome, the mutation SCN5AE555X was discovered. Therefore, cardiac sodium channelopathy pig models were generated by homologous recombination in the genetic background of outbred Yucatan minipigs via SCNT exhibiting the orthologous porcine heterozygous mutation SCN5AE558X. The heterozygous mutant animals were viable and fertile, and showed no sudden death over a 2-year monitoring period. They showed reduced SCN5A protein expression, which resulted in diminished total sodium conductance. The heterozygous mutant hearts showed slowed conduction and increased susceptibility for ventricular arrhythmias in the absence of structural defects of the myocardium or specialized conduction system. In total, a novel animal model was established for understanding the mechanisms linking sodium channel dysfunction to cardiac pathophysiology (Park et al., 2015b).

Melanotan II is a synthetic hormone that speeds up the production of melanin, the pigment that absorbs ultraviolet radiation and gives skin its colour. It was originally developed as a potential treatment for female sexual dysfunction and erectile dysfunction, but this research ceased in 2003. In technical terms, Melanotan II is a synthetic analogue of the peptide hormone α-melanocyte-stimulating hormone (α-MSH). Today, there are numbers of sellers on the internet of unlicensed and untested powders sold as Melanotan II.

Its unique potential as a healing substance lies in that it interacts with cellular actin and regulates its activity. Tb4 prevents actin from assembling (polymerizing) to form filaments but supplies a pool of actin monomers (unpolymerized actin) when a cell needs filaments for its activity. A cell cannot divide if actin is polymerized. Tb4 therefore serves in vivo to maintain a reservoir of unpolymerized actin that will be put to use when cells divide, move and differentiate.


I am not a doctor and nothing I say should be taken as medical advice. If you have a read through the article, I would suggest following the recommendations there. If you want to go into detail book a consult at
But what about the three-month warning? Dr Rush, while an advocate for the supplement, sees it as a short-term solution, and not something to rely on long-term, for good reason. "Technically taking 5-HTP alone can deplete important brain chemicals such as dopamine and adrenaline. While 5-HTP is aimed at increasing the amount of serotonin in the body, dopamine and adrenaline are also important for positive mental health states. In order to prevent the depletion of important brain chemicals, taking 5-HTP would need to be balanced with amino acids that support the production of dopamine and adrenaline." That's L-Tyrosine, which you eat in soy, chicken and beef, and can also be found in health food shops as a supplement.
Don’t take it by itself, you want to take it with a meal. The half life seems to vary; some people just need to take a single dose daily whereas some break it up into several doses. The dosage range is pretty wide, from 50 to 900 milligrams. Many report the antidepressant effect desired from lower doses, so start low with this one. Do not use a liquid form of 5-HTP.

Its unique potential as a healing substance lies in that it interacts with cellular actin and regulates its activity. Tb4 prevents actin from assembling (polymerizing) to form filaments but supplies a pool of actin monomers (unpolymerized actin) when a cell needs filaments for its activity. A cell cannot divide if actin is polymerized. Tb4 therefore serves in vivo to maintain a reservoir of unpolymerized actin that will be put to use when cells divide, move and differentiate.


MAPKs and NF-κB played pivotal roles in the development of osteoclasts downstream of RANK signaling [54]. In this study, we demonstrated that Tβ4 activation by Tβ4 peptide inhibited RANKL-induced p38, ERK, JNK MAPK, and NF-κB signaling pathways. These results suggested that Tβ4 activation might inhibit osteoclast differentiation via inhibition of the signaling cascades MAPK/NF-κB/NFATc1.

Cognitive impairment has repeatedly been described in bipolar disorders… Serotonin (5-hydroxytryptophan; 5-HT) is possibly involved in these cognitive processes, more particularly in executive functions, learning, memory, and attention. The aim of this study was to investigate serotonergic vulnerability and its relation to cognitive functioning in healthy first-degree relatives of [bipolar disorders] patients…


A: 5-HTP (5-hydroxy-tryptophan) 5-htp-5-hydroxytryptophan is converted to serotonin in the body. Because 5-HTP is related to serotonin, it should not be taken with drugs, which may affect serotonin level. These drugs are SSRI (selective serotonin reuptake inhibitors) such as Paxil (paroxetine), Zoloft (sertraline), Prozac (fluoxetine), Celexa (citalopram) and others. The list of drugs: Plavix (clopidogrel), Lipitor (atorvastatin), Uroxatral (alfuzosin), bisoprolol, aspirin and lisinopril do not affect serotonin in the body. Tramadol, however, has a weak inhibition of serotonin reuptake and can increase serotonin levels. It is therefore recommended that tramadol and 5-HTP be used with caution. The patient needs to be monitored for serotonin syndrome, which may include changes in mental status, tremor, hyperthermia, rigidity, seizure, increase sweating and shaky movement. The interaction may also cause a cerebral vasoconstrictive disorder such as Call-Fleming syndrome. It is important to discuss the use of tramadol and 5-HTP with your healthcare provider before taking 5-HTP. Lori Mendoza, RPh
Tβ4 is not a thymus-specific peptide but also present in most tissue and all cells except red blood cells [35]. High amounts of Tβ4 were detected in human white blood cells, especially in neutrophils and in macrophages [34], expressed in developing mandible (embryonic day 12) [36] and hair follicles (HF) of mice [37]. In addition, the peptide is also detected outside cells, in blood plasma and in wound and blister fluids [34]. Although the mechanism(s) of action of exogenous Tβ4 on anti-inflammatory effects remains unclear, the high levels of Tβ4 present in human wound fluid (13 μg/mL) suggest its importance in wound healing or anti-inflammation [38]. However, the level of Tβ4 is variable (unchanged, decreased, and increased) in GCF or biopsied gingival tissue of periodontal patients [20, 21]. Based on the observations that Tβ4 has anti-inflammatory effects [11–14], the hypothesis is that Tβ4 regulates inflammatory mediators and osteoclastogenesis in osteolytic bone disease, such as periodontitis.
The first dosage should be fairly small, as little as 0.3mg in order to gauge the reaction of the user's body. With increased dose first time user will deel warming ensation, flush in face and mild nausea, if these side effects occure dosage can be taken before going to bed, so any unpleasant effects take place while user is asleep. With regular use these side effects disapper and product can be taken at any tome of the day.
Hey mate, I’m getting a shoulder reconstrcution in about 2 weeks. Do you think that TB-500 and BPC-157 would help heal something as complex as this. Or do you think that stacking something like GHRP-6 and CJC-1295 would work better because this would assist in muscle growth and strength gains of surrounding muscles etc. Also if chose to use peptides when do you think I should start using them, I will be in a sling for 6weeks after surgery with only passive movements.
This article is authored by a PhD Candidate and her supervisory team at University of Queensland, and reflects the interests of the student’s doctoral project in undertaking the nation’s first qualitative study into experiences of Melanotan use among the general population. Dubbed ‘Project Melanotan’, the investigation aims to directly engage with ‘melanotanners’ in a non-judgemental environment, in an effort to both critically evaluate as well as understand lived experiences of melanotaning as they relate to conceptually relevant notions of risk, technology and the body.
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 ×