The matters under subsection 52E (1) of the Therapeutic Goods Act 1989 considered relevant by the delegate included: (a) the risks and benefits of the use of the substance; (b) the purposes for which a substance is to be used and the extent of use of a substance; (c) the toxicity of the substance; (d) the dosage, formulation, labelling, packaging and presentation of a substance; (e) the potential for abuse of a substance; and (f) any other matters that the Secretary considers necessary to protect public health.

Oxytocin production is controlled by a positive feedback mechanism. This mechanism allows the release of the oxytocin hormone when a trigger occurs. The hormone then causes an action in the body, such as the letdown of milk or the start of labor contractions, which signals more production of oxytocin. The feedback cycle continues until the action, such as childbirth or feeding the baby, is complete.
Melanotan II is a synthetic analogue of the α-melanocyte stimulating hormone (α-MSH). α-MSH is a melanocortin I receptor agonist which has a role in human pigmentation by stimulating production of eumelanin. As melanotan II is a non-specific melanocortin receptor agonist, it has been reported to cause toxicity effects involving the many physiological systems affected by the receptors.
Bonding. In the Prairie Vole, oxytocin released into the brain of the female during sexual activity is important for forming a monogamous pair bond with her sexual partner. Vasopressin appears to have a similar effect in males. In people, plasma concentrations of oxytocin have been reported to be higher amongst people who claim to be falling in love. Oxytocin has a role in social behaviors in many species, and so it seems likely that it has similar roles in humans.6
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 (CRH) and dynorphin, for example, that act locally. The magnocellular neurons that make oxytocin are adjacent to magnocellular neurons that make vasopressin, and are similar in many respects.
Guastella and his team just completed an unpublished study that is the first to test the effects of oxytocin on couples in therapy. In one part of the study, couples were asked to discuss a “hot topic,” one that usually led to conflict between the pair, and to then try to solve the issue. Although the data analysis is still in progress, Guastella expects couples that got oxytocin to show less hostile interpretations of the problem and be less critical of their partners. He thinks overall it will increase perspective-taking and reduce blame, leading to smoother communication and better problem-solving.
In the male mammal, the small peptide hormone oxytocin is produced in similar quantities within the hypothalamo-pituitary magnocellular system as in the female, yet for the male little is known about the physiology associated with this hormone. The present review summarizes what is known about the function of oxytocin in the male mammal and tries to take account of both central and systemic effects, and those linked with a local production of oxytocin within the male reproductive organs. In several species a pulse of systemic oxytocin, presumably of hypothalamic origin, appears to be associated with ejaculation. The systemic hormone could act peripherally stimulating smooth muscle cells of the male reproductive tract, but could also reflect central effects in the brain modulating sexual behaviour. In addition to systemic oxytocin, the peptide is also made locally within the testis, and possibly also the epididymis and prostate. In the former tissue it appears to have an autocrine/paracrine role modulating steroid metabolism, but may in addition be involved in contractility of the seminiferous tubules. However, the latter function may involve the mediacy of Sertoli cells which under some circumstances can also exhibit the components of a local oxytocin system. In the prostate of the rat and the dog oxytocin is linked again to steroid metabolism and may also act as a growth regulator. Finally, oxytocin in seminal fluid is discussed and its possible role in respect to the fate of the semen following ejaculation.
In conclusion, this study is the first study to demonstrate that down-regulation of Tβ4 was observed in an in vitro model of H2O2-stimulated PDLCs. Tβ4 activation had anti-inflammatory effects via MAPK and NF-κB pathways in PDLCs and anti-osteoclastogenic effects via MAPK, NF-κB, and Wnt5a pathways in BMMs. These findings supported the fact that Tβ4 peptide could possibly be used in the development of a therapeutic drug for periodontitis and osteolytic disease.
On the most basic level, a peptide is essentially a small protein. Billions of unique peptides exist, all with different effects and functions in the body. Physiological examples include insulin, oxytocin, and casein, the main protein in milk. Thus, to taunt Essendon supporters for the use of “peptides” is rather non-specific. A much more intelligent insult would be to focus on the administration of thymosin beta-4.
Oxytocin is known as the hormone that promotes feelings of love, bonding and well-being. It's even being tested as an anti-anxiety drug. But new research shows oxytocin also can cause emotional pain. Oxytocin appears to be the reason stressful social situations, perhaps being bullied at school or tormented by a boss, reverberate long past the event and can trigger fear and anxiety in the future. That's because the hormone actually strengthens social memory in the brain.

Bartz found that when she averaged out the volunteers’ results, the sniffs of oxytocin hadn’t seemed to colour their memories of their mothers. But things changed when she looked at them individually. Those who felt more anxious about their relationships took a dimmer view of their mother’s parenting styles when they sniffed oxytocin, compared to the placebo. Those who were more secure in their relationships reacted in the opposite way – they remembered mum as being closer and more caring when they took the oxytocin.
To investigate whether the newborn neurons generated in the DG are capable of projecting their axons into the CA3 region of the hippocampus after TBI, we stereotactically injected a fluorescent tracer, 1,1″-dioleyl-3,3,3″,3″-tetramethylindocarbocyanine methanesulfonate (Dil, Delta 9-DiI; AnaSpec, San Jose, CA) into the ipsilateral CA3 region (stereotaxic coordinates AP, -3.6 mm bregma, ML, 3.6 mm, DV, 3.0 mm, Paxinos and Watson, 1994) at day 28 after TBI. BrdU (100mg/kg, ip) was injected i.p. daily starting at day 1 after TBI for 10 days to label newly generated cells. One week after DiI injection (i.e., 35 days after TBI), the animals were anesthetized and sacrificed. Their brains were fixed in 4% paraformaldehyde. The brain was cut into seven equally spaced 2-mm coronal blocks using a rat brain matrix. The brain blocks containing the hippocampus were processed for vibratome sections (100 μm) followed by BrdU staining. BrdU and DiI labeling in the hippocampus on brain sections was analyzed with a Bio-Rad MRC 1024 (argon and krypton) laser-scanning confocal imaging system mounted onto a Zeiss microscope (Bio-Rad, Cambridge, MA). Co-localization of BrdU-positive nuclei within retrogradely DiI-labeled granule cells was found, indicating that newborn granule neurons extend axons into the CA3 region that are capable of retrogradely transporting DiI from the CA3 to their cell bodies within the DG after TBI (Fig.2). This finding suggests that newborn granule neurons may be incorporated into functional hippocampal circuitry after TBI.
This sounds very promising and I have a question I’m sure you haven’t heard before. It’s regarding healing. I’m about 230 and avid lifter as well as running occasionally. But I’ve had severe injuries to my l3-s1 for years a d yes I’ve tried some stuff before as far as lifting. But when I was 2 I had encephalitis. I survived it back in 74 which most didn’t however the treatment had left me with migraines and seizures as a child and was told my adult teeth would be very weak when they grew in. So I’m 44 and most of my teeth have broken and I’ve been looking for alternatives to implants. You said both the products mentioned in this article would improve healing and I’ve heard stem cells are capable of regrowing teeth. Would this work for me and how or where would I inject it or maybe do a oral form and let it sit in my mouth for a bit? Never really thought about this but I’ve tried so many clinical trials and been turned down each time. Any info would be greatly appreciated thank you in advance.
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As shown in Figure 1, thymic hormones also modulate the production of hypothalamus pituitary hormones and neuropeptides. Initial experiments revealed that neonatal thymectomy promotes a decrease in the number of secretory granules in acidophic cells of the adenopituitary [44]. In the same vein, athymic nude mice display low levels of various pituitary hormones, such as PRL, GH, LH and FSH [45]. With regard to thymic peptides, thymosin beta-4, when perfused intraventricularly, stimulates LH and LHRH secretion [46]. Similar results were obtained with another thymic peptide, thymulin, in perfused or fragmented pituitary preparations [47]. The administration of thymopoietin (another chemically-defined thymic hormone) in children with Hodgkin’s disease increased GH and cortisol serum levels [48]. Moreover, thymopentin (the synthetic biologically active peptide of thymopoietin) enhances in vitro the production of ACTH and beta-endorphin [49]. In addition, thymulin exhibits an in vitro stimulatory effect on perfused rat pituitaries, enhancing PRL, GH, TSH and LH release [50]. Using short-term cultures of pituitary fragments, an increase in ACTH secretion occurs after in vitro thymulin addition, with no changes in GH levels and significant reductions in PRL release [47]. A further thymosin peptide was recently isolated with the task in stimulating IL-6 release from rat glioma cells [51]. By contrast, thymosin alpha-1 is apparently able to down regulate TSH, ACTH and PRL secretion in vivo with no modifications on GH levels [52]. These inhibitory effects seem to occur through hypothalamic pathways. Indeed, the production of the corresponding releasing hormones by hypothalamic neurones decreased after in vitro addition of thymosin alpha-1 in medial basal hypothalamic fragments [52].
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.
The neurotransmitter serotonin is synthesized from the amino acid tryptophan through 5-HTP. In which tryptophan gets converted into 5-HTP via the enzyme tryptophan hydroxylase and 5-HTP gets converted into serotonin via the enzyme L-amino acid decarboxylase.[4] Serotonin is later degraded into 5-hydroxyindoleacetic acid (5-HIAA) by monoamine oxidase.
Cells were pretreated with indicated concentrations of Tβ4 peptide for 2 hours and then incubated with 200 μM H2O2 for 48 hours (A, B). The mRNAs expression was examined by RT-PCR analysis. This data were representative of three independent experiments. The bar graph shows the fold increase in mRNA expression compared with control cells. * Statistically significant differences compared with the control, p<0.05.
Jump up ^ Ballweber E, Hannappel E, Huff T, Stephan H, Haener M, Taschner N, Stoffler D, Aebi U, Mannherz HG (Jan 2002). "Polymerisation of chemically cross-linked actin:thymosin beta(4) complex to filamentous actin: alteration in helical parameters and visualisation of thymosin beta(4) binding on F-actin". Journal of Molecular Biology. 315 (4): 613–25. doi:10.1006/jmbi.2001.5281. PMID 11812134.
In another study, published in PNAS in 2010, men were given a dose of oxytocin and asked to write about their mothers. Those with secure relationships described their moms as more caring after the hormone dose. Those with troubled relationships actually saw their mothers as less caring. The hormone may help with the formation of social memories, according to the study researchers, so a whiff strengthens previous associations, whether good or bad.
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.

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My mother was a mother of 6 born between 1948 and 1961. She was a great advocate for lots of cuddles and physical contact with all of her children (as was my dad). This included baby massage directly on the skin as she emphasised touch as being very important. She passed this knowledge onto me when I became an aunt and then a mother. I am very grateful to have had such a hands on, affectionate and intuitive mother as a role model.
The soluble form of Ac-SDKP peptide, derived from thymosin beta-4, has been described as a natural inhibitor of pluripotent hematopoietic stem cell proliferation and as a stimulator of angiogenesis, both in vitro and in vivo (Koutrafouri et al., 2001; Wang et al., 2004). This peptide has been selectively bound to acrylated hyaluronic acid hydrogels via thiol groups from cysteine residues (Song et al., 2014). Unfortunately, the immobilization process was poorly characterized and the effect of hydrogels on EC function was not tested in vitro. In a mouse model of chronic myocardial infarction, hydrogels with immobilized Ac-SDKP did not show improved regeneration potential. Yet, Ac-SDKP-HA hydrogels with entrapped stem cell homing factor SDF-1 showed a significant increase of myocardial regeneration and recovery of heart function, as compared to groups with only one or none of these factors, suggesting a potentially interesting synergistic effect.
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).
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).
This may be an odd question. But would this be good to inject or spray on those that have undergone hair transplants in the first month of surgery. Fue microscars. I see you mention it improves hair growth and blood flow. both which basically what rogaine claims to do. Surely this would benefit new transplanted hair follicles in taking and holding? Interested in your thoughts in the matter.
In humans, 5-HTP is the nutrient precursor to the neurotransmitter serotonin – widely known as the 'happy neurotransmitter' – meaning 5-HTP converts directly into serotonin in the brain. As well as being in our bodies, it's found naturally in the seeds of a woody shrub native to West Africa. By taking it as a supplement, in theory, you will end up with more serotonin in your brain. Serotonin deficiency is linked to depression, anxiety and a whole host of physical and mental ailments. Raising its levels seems to help brain cells send and receive chemical messages, which in turn boosts mood.
The neurotransmitter serotonin is synthesized from the amino acid tryptophan through 5-HTP. In which tryptophan gets converted into 5-HTP via the enzyme tryptophan hydroxylase and 5-HTP gets converted into serotonin via the enzyme L-amino acid decarboxylase.[4] Serotonin is later degraded into 5-hydroxyindoleacetic acid (5-HIAA) by monoamine oxidase.
I’ve used powdered 5-HTP a couple times now, it doesn’t taste great and it’s resulted in an unpleasant stomach upset that lasted 45–60 minutes. For that reason I’ll likely not continue to use it. I did not find it’s effect on mood remarkable enough that I would want to put up with the stomach upset. My go to Nootropics for mood are Rhodiola and Phenibut and my go to Biohacks for mood are meditation and no fap, I don’t feel the need to use a whole lot more mood promoting strategies.

At least one study has actively differentiated between 'an increase in satiety' (sensation of fullness from food) and a 'decrease in appetite' (less desire to eat) and noted that 5-HTP causes an increase in satiety without a concomitant decrease in appetite.[9] Additionally, most studies are in exclusively females which may have more significance with interventions pertaining to serotonin metabolism; only one study mentioned above was conducted in men as well[10] but appears to suggest that it benefits both genders.
The full-length Tβ4 polypeptide has been shown to be effective in reducing inflammation [44]. It is also reported that only the 4-AA, amino-terminal peptide of Tβ4, known as Ac-SDKP, can block inflammation [45]. In this study, we used a synthetically human peptide produced copy of a naturally occurring, highly conserved 43-amino acid (MW = 4964 Da) water soluble acidic peptide, originally isolated from bovine thymus tissue [46]. This peptide is produced by Fmoc solid-phase peptide synthesis in accordance with the current Good Manufacturing Practice (cGMP) regulations (21 CFR 210 and 211) of the FDA [47]. An effective healer, Tβ4 can be administered topically on the surface of cells and systemically, through injection [9–11]. In this study, Tβ4 activation by Tβ4 peptide inhibited H2O2-induced production of NO and PGE2, expression of COX-2 and iNOS, and mRNA expression of TNF- α, IL-1β, -6, -8, and -17 in cultured PDLCs. These findings suggested that Tβ4 activation possessed anti-inflammatory activity in PDLCs. These results were consistent with previous in vivo and in vitro studies [9–15]. MAPK is a proline-directed serine/threonine kinase consisting of three-enzyme modules; its targets, inducing ERK, JNK and p38 kinases, are important in cellular signal transduction pathways and exert an anti-inflammatory response [48, 49]. NF-κB is a major transcription factor involved in the release of proteins that mediate the inflammatory response, and the degradation and phosphorylation of Iκ-Bα are necessary to release NF-κB from the cytoplasmic NF-κB/Iκ-Bα complex and allow its subsequent translocation to the nucleus of the cell [50]. In this study, Tβ4 peptide down-regulated the H2O2-triggered activation of the ERK and JNK MAPKs and the NF-κB in PDLCs. These results suggested that the ERK and JNK MAPKs and the NF-κB pathway may be involved in the anti-inflammatory effects of Tβ4 activation in PDLCs. Consistent with our findings, Tβ4 treatment decreased TNF-α-induced NF-κB activation in human corneal epithelial cells [51].
James Bates* who recently started taking it for panic attacks, said, "A friend who had anxiety recommended 5-HTP to me. I used to take beta-blockers and Valium but the doctors have got funny about giving them to me. I needed an alternative and didn't fancy getting back on Prozac. I've only been taking the supplements for a month but so far, it's helped a lot. I've only had two panic attacks, whereas usually I'd have four or five."
Before the treatment, the female mice were largely indifferent to the cries of a distressed baby, and were even known to trample over them. But after an injection of oxytocin, the mice started to respond more like mothers, picking up the mewling pup in their mouths. Froemke, a neuroscientist at New York University's Langone Medical Center in New York City, was monitoring the animals' brains to find out why that happened.
Toxicity effects of melanotan II from therapeutic and overdose exposures include renal dysfunction, rhabdomyolysis, sympathomimetic overdrive, change in size and pigmentation of pre-existing moles, rapid increase in the number of new moles, associated with causing melanomas, posterior reversible encephalopathy syndrome, refractory priapism, stretching and yawning syndrome, shortness of breath, chest pain, abdominal cramping and pain, dizziness and lethargy.
5-HTP is POSSIBLY SAFE when taking by mouth appropriately. 5-HTP has been used safely in doses up to 400 mg daily for up to one year. However, some people who have taken it have developed a condition called eosinophilia-myalgia syndrome (EMS), a serious condition involving extreme muscle tenderness (myalgia) and blood abnormalities (eosinophilia). Some people think EMS might be caused by an accidental ingredient or contaminant in some 5-HTP products. However, there is not enough scientific evidence to know if EMS is caused by 5-HTP, a contaminant, or some other factor. Until more is known, 5-HTP should be used cautiously.
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