Again, the three groups of mice were exposed to the stressful experience of social defeat in the cages of other more aggressive mice. This time, six hours after the social stress, the mice were put in a box in which they received a brief electric shock, which startles them but is not painful. Then 24 hours later, the mice were returned to the same box but did not receive a shock.
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.
But this isn’t the only study to show the subtle side of oxytocin. Just three months ago, I wrote about research from Heejung Kim at the University of California, which showed how oxytocin’s effects vary across different cultures. To fulfil its many roles, oxytocin has to dock at a protein called the ‘oxytocin receptor’, encoded by a gene called OXTR.
Oxytocin is known to be metabolized by the oxytocinase, leucyl/cystinyl aminopeptidase.[25][26] Other oxytocinases are also known to exist.[25][27] Amastatin, bestatin (ubenimex), leupeptin, and puromycin have been found to inhibit the enzymatic degradation of oxytocin, though they also inhibit the degradation of various other peptides, such as vasopressin, met-enkephalin, and dynorphin A.[27][28][29][30]
Uterine contractions. These are important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.16
The cornea is the outer thin layer of epithelial cells protecting the eye. After wounding, timely resurfacing of the cornea with new cells is critical, to prevent loss of normal function and loss of vision. Corneal epithelial healing occurs in stages, with cells migrating, dividing and differentiating. Therapies for corneal injury are limited. Therefore, the recent finding that Tb4 promotes corneal wound repair in animal models offers hope for a therapeutic product that will improve the clinical outcome of patients with injured corneas.
What to know about hormonal imbalances While it is natural to experience hormonal imbalances at certain times in life, such as puberty, menopause, and pregnancy, some hormonal changes are related to underlying medical conditions. This article looks at the causes and symptoms of hormonal imbalances in men and women, as well as treatment and home remedies. Read now

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.

Indeed, the findings that progenitor cells of some form exist both in the regenerative zebrafish heart, and in the hearts of less-regenerative mammals supports this idea. Zebrafish have ostensibly found some method to optimize the activity of progenitor cells, perhaps either by maintaining more cells, or by harboring a more cultivating environment for regeneration. Also, both mammalian and nonmammalian hearts contain an epicardial cell layer, yet zebrafish have found some way to activate the epicardium after injury, a process linked with essential neovascularization of regenerating muscle (Lepilina et al., 2006. This result points to the adult mammalian epicardium as a potential cellular source to assist myocardial regeneration or survival. Indeed, mammalian myocardial infarcts typically show poor or insufficient neovascularization, a response that many are trying to improve experimentally. Recent findings have indicated that the G-actin sequestering protein, Thymosin-ß4, may influence the mammalian epicardium. Treatment of adult cardiac explants with Thymosin-ß4 induced the migration of fibroblasts, endothelial and smooth muscle cells as assessed by gene expression and cellular morphology (Smart et al., 2007). In addition, in vivo Thymosin-ß4 treatment could partially restore cardiac survival and function following coronary ligation (Bock-Marquette et al., 2004). Notably, Thymosin-ß4 expression is induced in the injured zebrafish heart, suggesting that fish naturally release this epicardial stimulant on injury (Lien et al., 2006).

Expanding upon the possible anti-panic effects of 5-HTP, one study using 2mg/kg 5-HTP to children (3.2-10.6 years of age) at bedtime for 20 days noted that 5-HTP was asssociated with beneficial response (more than 50% reduction in night terror frequency) of 93.5% of children relative to 28.6% in placebo.[42] Oddly, 6 months after the initial supplementation period the 5-HTP group still reported less sleep terrors (83.9% reporting improvement).[42]
For this study, one of us, Ben Trumble, followed Tsimane men as they went hunting for food. Typically, Tsimane men set out alone or with a partner in the early morning and search in the forest for prey such as wild pigs, deer, monkeys, or the rare tapir. Following long looping trails they might be gone for eight or nine hours, traveling about six miles (ten kilometers). Ben collected saliva samples throughout the hunt in order to measure changes in men’s hormone levels.
“Shortly after taking the supplement, my vision changes. Colours appear more vivid, I feel lightheaded and generally at ease. My mind calms down and the racing thoughts stop. Today is the 3rd day and I’ve noticed the intensity has gone up and it almost feels like I’m tripping on something. The sky looked absolutely amazing today, colours are so intense but I feel a kind of ungrounded and odd, but still pretty mellow with no anxious thoughts or anything like that which is good.”
Oxytocin affects social distance between adult males and females, and may be responsible at least in part for romantic attraction and subsequent monogamous pair bonding. An oxytocin nasal spray caused men in a monogamous relationship, but not single men, to increase the distance between themselves and an attractive woman during a first encounter by 10 to 15 centimeters. The researchers suggested that oxytocin may help promote fidelity within monogamous relationships.[109] For this reason, it is sometimes referred to as the "bonding hormone". There is some evidence that oxytocin promotes ethnocentric behavior, incorporating the trust and empathy of in-groups with their suspicion and rejection of outsiders.[66] Furthermore, genetic differences in the oxytocin receptor gene (OXTR) have been associated with maladaptive social traits such as aggressive behavior.[110]
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.[13] 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.
A number of factors can inhibit oxytocin release, among them acute stress. For example, oxytocin neurons are repressed by catecholamines, which are released from the adrenal gland in response to many types of stress, including fright. As a practical endocrine tip - don't wear a gorilla costume into a milking parlor full of cows or set off firecrackers around a mother nursing her baby.
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).

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).
I have done my research related to this, I am thinking about ordering TB-500…I have a few questions to ask before ordering, I am a volleyball player and stopped playing for a while to let it rest and in process of healing. I have A SLAP tear is an injury to the labrum of the shoulder. Should I use TB-500 for shoulder so it can increase muscle growth? I would be interested on your take of how to do the injections there.
Cardiac effects: oxytocin and oxytocin receptors are also found in the heart in some rodents, and the hormone may play a role in the embryonal development of the heart by promoting cardiomyocyte differentiation.[50][51] However, the absence of either oxytocin or its receptor in knockout mice has not been reported to produce cardiac insufficiencies.[49]
Cells were pretreated with indicated concentrations of Tβ4 peptide for 2 hours and then incubated with 200 μM H2O2 for 48 hours (A-C). Protein expressions were assessed by Western blot analysis (A). The production of NO (B) and PGE2 (C) were measured by Griess reaction and ELISA, respectively. Data replicated the quantifications of NO and PGE2 with the standard deviation of at least three experiments (n = 4). The bar graph shows the fold increase in protein expression compared with control cells. * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2—treated group.
Silencing of the Tβ4 or Wnt5a gene was achieved by transfecting cells with small interfering RNA (siRNA). Cells were transfected with Tβ4 or Wnt5a siRNAs (30 nM) for 24 hours using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's instructions. Cells were transfected with Silencer negative control siRNA using the same protocol.
It has been noted[25] that isolated supplementation of 5-HTP may deplete or reduce the bioactivity of catecholamines such as dopamine[44][45][46] (which extends to L-Tryptphan[45]) and that this relationship also acts in reverse, with supplemental L-Tyrosine possibly able to deplete 5-HTP[47][48] and Serotonin itself,[48] which extends to supplemental L-DOPA which may reduce all intermediate of serotonin synthesis[49][50][51] although L-DOPA may also deplete L-Tyrosine (as it is merely later in the same metabolic chain).[50] Due to excessive levels of either one depleting the other, some authors have suggested that combination therapy of 5-HTP and L-Tyrosine (the furthest back in the metabolic chain while still passing rate limiting enzymes) is a potentially useful avenue for anti-depressive effects.[52]
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.
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
A NOTE ABOUT RELEVANT ADVERTISING: We collect information about the content (including ads) you use across this site and use it to make both advertising and content more relevant to you on our network and other sites. This is also known as Online Behavioural Advertising. You can find out more about our policy and your choices, including how to opt-out here.
Despite these many roles, oxytocin is often reduced to a misleading label. While “hormone of love” may be great for catchy headlines and compelling marketing slogans, they are ultimately misleading. Jennifer Bartz from the Mount Sinai School of Medicine has found that oxytocin can have completely opposite effects on the way people behave, depending on how they view their relationships to other people.
I was kind of scared because I ran across some threads that said TB500 leads to cancer or promotion of benign tumors…most of these were at least 4-5 years old though and it seems there are countless logs online all with good experiences. Nonetheless I was still worried so I did some more research and came across a pharmaceutical company in the US doing clinical trials for thymosin beta 4 to help with dry eye syndrome. I have attached some links. This makes me feel much safer but if you have any more insight I’d really appreciate it.
Maintenance doses are taken once the desired pigmentation has been reached and requires much less frequent dosing. Unfortunately, this is where too many variables come into play to give exact instructions. Skin type, bodyweight, metabolism regulating speed of skin fading, uv ray exposure, preferred tan level – all that makes impossible to give correct advice on maintenance dose. Everyone will find their own perfect dose and dosing frequency through some trial and error. To not leave you completely disinformed on this subject here is example of loading and maintenance which can be used as starting point where to adjust from:
Thymosin beta-4 is a naturally occurring peptide, and is found ubiquitously in our cells. A range of studies on animal models have indicated several key biological activities for Tβ4, such as “promot[ing] wound repair, tissue protection, and regeneration in the skin, eye, heart and central nervous system”. Only a handful of clinical trials in humans have attempted to explore these roles practically.
A warning: unlike BPC-157, TB-500 is absolutely, 100% banned by WADA and most other global sporting organization both in-competition and out-of-competition. You should NOT use this if you are competing in any such sanctioned sport as it definitely falls under the banned category of “Peptide Hormones, Growth Factors, Related Substances and Mimetics (S2)”.
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
Tβ4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners. Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs. Tβ4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-κB in PDLCs. Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs. In addition, H2O2 up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2 in PDLCs. Wnt5a inhibition by Wnt5a siRNA enhanced the effects of Tβ4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.
Oxytocin produces antidepressant-like effects in animal models of depression,[81] and a deficit of it may be involved in the pathophysiology of depression in humans.[82] The antidepressant-like effects of oxytocin are not blocked by a selective antagonist of the oxytocin receptor, suggesting that these effects are not mediated by the oxytocin receptor.[17] In accordance, unlike oxytocin, the selective non-peptide oxytocin receptor agonist WAY-267,464 does not produce antidepressant-like effects, at least in the tail suspension test.[83] In contrast to WAY-267,464, carbetocin, a close analogue of oxytocin and peptide oxytocin receptor agonist, notably does produce antidepressant-like effects in animals.[83] As such, the antidepressant-like effects of oxytocin may be mediated by modulation of a different target, perhaps the vasopressin V1A receptor where oxytocin is known to weakly bind as an agonist.[84][85]
I’ve been on this stuff for lots of years. I really needed it when I was depressed like hell, and I had an emotional pain that simply didn’t go away for 2 decades prior to starting that stack. Did it help? yes. Was it the best intervention possible? probably not. I was able to get off all this stuff with the uridine stack, and I believe it partly fixed a part of my brain that was damaged from this decade long suffering. So this is, why I am now more into brain regeneration and psychotherapeutic interventions (even though I do them myself), and I would only go back to this stack if I was completely fucked up again. There are a lot of side effects, and its a fine line to balance the supplements, to get rid of the side effects…

Hypoxic heart disease is a predominant cause of disability and death worldwide. As adult mammals are incapable of cardiac repair after infarction, the discovery of effective methods to achieve myocardial and vascular regeneration is crucial. Efforts to use stem cells to repopulate damaged tissue are currently limited by technical considerations and restricted cell potential. We discovered that the small, secreted peptide thymosin beta4 (Tbeta4) could be sufficiently used to inhibit myocardial cell death, stimulate vessel growth, and activate endogenous cardiac progenitors by reminding the adult heart on its embryonic program in vivo. The initiation of epicardial thickening accompanied by increase of myocardial and epicardial progenitors with or without infarction indicate that the reactivation process is independent of injury. Our results demonstrate Tbeta4 to be the first known molecule able to initiate simultaneous myocardial and vascular regeneration after systemic administration in vivo. Given our findings, the utility of Tbeta4 to heal cardiac injury may hold promise and warrant further investigation.

Adam Guastella, a clinical psychologist at University of Sydney’s Brain and Mind Research Institute, and a pioneer in studies of how oxytocin can help people with autism, thinks the hormone can also help people in couple therapy by facilitating empathic communication. His research has shown that people who get oxytocin are more focused on positive emotion: they remember happy faces better than angry and neutral ones. Research by others has shown that oxytocin increases trust, generosity and our ability to identify emotion in facial expressions. It is perhaps by these mechanisms that the hormone improves communication.
Tβ4 is a multifunctional regenerative small peptide containing 43-amino acids, and it is the major G-actin-sequestering molecule in eukaryotic cells.21 Tβ4 has pro-survival and pro-angiogenic properties, protects tissue against damage, and promotes tissue regeneration.22,23 It also plays a key role in corneal, epidermal and cardiac wound healing.21 Tβ4 participates in axonal path-finding, neurite formation, cell proliferation, and neuronal survival.24-26 Our previous studies show that Tβ4 reduces inflammation and stimulates remyelination and improves functional recovery in animal models of experimental autoimmune encephalomyelitis (EAE) and stroke.25,27 In summary, these pleiotropic properties make Tβ4 an ideal candidate for treatment of TBI.
In some studies that record appetite suppression with 5-HTP supplementation, nausea appears to also be reported at higher freqencies than placebo,[9] although some interventions note this as the only relevant side effect.[10] Short term studies tend to note that nausea persists throughout the study period[10] while those expanding beyond three weeks note that reports of nausea tend to decline at this time point.[9]
It would have been interesting if Bartz had asked about *both* parents’ parenting styles. (Spoken by a guy writing a book on fathers.) It would have been easy enough; just add another question. Any differences between perceptions of mothers and fathers might have been illuminating. But, as in so much family research, fathers were once again ignored or excluded. (As if fathers don’t have parenting styles…)
This anti-social effect of a social hormone brings some nuance to the story of oxytocin. In one study, researchers found that Dutch students given a snort of the hormone became more positive about fictional Dutch characters, but were more negative about characters with Arab or German names. The finding suggests that oxytocin's social bonding effects are targeted at whomever a person perceives as part of their in-group, the researchers reported in January 2011 in the journal PNAS.
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.
Another interesting agent reported to significantly accelerate chronic wound repair is infrared (700–1200 nm wavelength) and near infrared (600–700 nm) light delivered through lasers or light-emitting diodes (LEDs) (Mester et al., 1968; Rochkind et al., 1989; Conlan, 1996; Schindl et al., 2000; Enwemeka, 2004). Spectroscopic measurements indicate that photons at wavelengths of 630–800 nm penetrate through the skin and muscles of the forearm and lower leg (Chance et al., 1988; Beauvoit et al., 1994, 1995). The effect of the light may be to stimulate cytochrome c oxidase in the mitochondria, resulting in increased oxygen consumption and production of ATP (Karu, 1999).
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.
These proteins, which typically contain 2-4 repeats of the β-thymosin sequence, are found in all phyla of the animal kingdom, with the probable exception of sponges[21] The sole mammalian example, a dimer in mice, is synthesised by transcriptional read-through between two copies of the mouse β15 gene, each of which is also transcribed separately.[22] A uniquely multiple example is the protein thypedin of Hydra which has 27 repeats of a β-thymosin sequence.[23]

The tb-500 has a systematic effect regardless of where it is injected. Some believe that thymosin beta-4 should be injected as close to the injury as possible however there is no evidence to show this would be superior. It can be injected subcutaneously (stomach fat) or intramuscularly (shoulders, thighs, buttocks). Injections should be given in different sites (rotated) each time. Depending on the spot, you can either feel nothing or you can feel slight pain - you will learn your favorite spots in time.
A study published last year in Biological Psychiatry was the first to assess whether people with variations in their oxytocin-receptor gene have a harder time maintaining romantic relationships than those who don’t. Hasse Walum, a graduate student at Karolinska Institute in Stockholm, and his colleagues took advantage of Swedish twin studies that included thousands of participants, their genetic information and their answers to questions about how affectionate they were with their romantic partners. They found that women with a specific variation weren’t as close to their partners as women without it: they kissed their partners less and didn’t desire physical proximity as often. These women were also more likely to report having had a marital crisis. Although researchers don’t know exactly how this variation affects the oxytocin system, it may result in a lower number of oxytocin receptors in the brain. People with fewer receptors would be less sensitive to the hormone’s effects.
People are using 5-HTP for absolutely everything from sleep disorders to OCD symptoms. After asking people in mental health Facebook groups whether they used it and why, I was inundated with responses. Sach Tennant, from London, takes it for her PMDD (premenstrual dysphoric disorder). "I only take it when I feel low and it only takes one hour to feel calm," she told me. "This month I only needed one to feel better. I don't get the zombie antidepressant feeling – you still have your emotions. Sleep is good on it. I used to have an inner voice that was male and used to bully me during PMT time. Noises seemed too loud, even like somebody eating a bag of crisps. Topping up with 5-HTP has stopped all this."

Exposure to ultraviolet (UV) light prompts an increased release of Alpha-MSH, which in turn stimulates the production of melanin in the skin. The more melanin produced the greater pigmentation level becomes, making the skin progressively darker and tan lasts significantly longer. This makes Melanotan peptide unique, people do not require as much exposure to UV light to produce more melanin, very attractive for people wishing to develop greater tanning of the skin in fastest way possible.
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.
Research substantiates Wiebe's anecdotal claims., 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.

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]
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
But Carter and other scientists are concerned by reports from the physicians and parents of children with autism spectrum disorder who say that they are already using oxytocin off-label — before it has been thoroughly tested. “We do not understand how the hormone works yet, or have enough information about what happens when it's given repeatedly,” Carter says. “This is not a molecule that people should be self-administering or playing with.”
But this isn’t the only study to show the subtle side of oxytocin. Just three months ago, I wrote about research from Heejung Kim at the University of California, which showed how oxytocin’s effects vary across different cultures. To fulfil its many roles, oxytocin has to dock at a protein called the ‘oxytocin receptor’, encoded by a gene called OXTR.

The RANKL and OPG have been identified as a key regulatory component of alveolar bone loss associated with inflammatory periodontal disease [52]. Moreover, PDLCs were shown to express several osteoclastogenic cytokines, including both OPG and RANKL [30, 31]. Our data demonstrated that Tβ4 peptide abolished H2O2-induced RANKL expression and restored OPG expression. Osteoclasts, bone-resorptive multinucleated cells derived from hematopoietic stem cells, are associated with osteolytic diseases. Furthermore, NFATc1, a master modulator of osteoclastogenesis, regulates target genes, such as cathepsin K and calcitonin receptor or Calcr [53]. In our in vitro study using BMMs, Tβ4 peptide directly and indirectly inhibited RANKL-induced osteoclast differentiation and expression of osteoclast markers, such as cathepsin-K, calcitonin receptor or Calcr, NFATc1, and RANK in BMM cells. These results indicated that Tβ4 was a key therapeutic target in controlling inflammation-induced bone loss.

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..