In a landmark 1979 study3, Cort Pedersen and Arthur Prange at the University of North Carolina in Chapel Hill showed that giving oxytocin to virgin rats could trigger maternal behaviours: the animals would build nests, lick or crouch over unfamiliar pups and even return lost pups to the nest. Researchers went on to show that oxytocin signalling in the brains of prairie voles (Microtus ochrogaster) helps the animals to form lifelong pair bonds4 — a rarity among mammals. In 2012, researchers even found a version of oxytocin in the tiny roundworm Caenorhabditis elegans, where it helps the animals find and recognize mates5.
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.
At least one study using an extract of Griffonia simplicifolia (10.24mg giving 2.56mg 5-HTP; confounded with Centella asiatica and Taraxacum officinale at 11.7mg and 4.55mg Paulina cupana and 9.75mg Artichoke extract) taken in three hits, five times a day (40mg 5-HTP total), by 20 overweight or obese females (non-depressive and without eating disorders) for 4 weeks has noted an increase in satiety and reduced binge eating tendencies; the increase in satiety was said to account for the improved weight loss results seen in the experimental group when both were given weight loss advice and diets.[3] This spray has been noted elsewhere to increase satiety (and vicariously through that, body weight) over 2 months in a similar demographic of women.[2]
Oxytocin is not only correlated with the preferences of individuals to associate with members of their own group, but it is also evident during conflicts between members of different groups. During conflict, individuals receiving nasally administered oxytocin demonstrate more frequent defense-motivated responses toward in-group members than out-group members. Further, oxytocin was correlated with participant desire to protect vulnerable in-group members, despite that individual's attachment to the conflict.[64] Similarly, it has been demonstrated that when oxytocin is administered, individuals alter their subjective preferences in order to align with in-group ideals over out-group ideals.[65] These studies demonstrate that oxytocin is associated with intergroup dynamics. Further, oxytocin influences the responses of individuals in a particular group to those of another group. The in-group bias is evident in smaller groups; however, it can also be extended to groups as large as one's entire country leading toward a tendency of strong national zeal. A study done in the Netherlands showed that oxytocin increased the in-group favoritism of their nation while decreasing acceptance of members of other ethnicities and foreigners.[66] People also show more affection for their country's flag while remaining indifferent to other cultural objects when exposed to oxytocin.[67] It has thus been hypothesized that this hormone may be a factor in xenophobic tendencies secondary to this effect. Thus, oxytocin appears to affect individuals at an international level where the in-group becomes a specific "home" country and the out-group grows to include all other countries.
Horvath, G. A., Stockler-Ipsiroglu, S. G., Salvarinova-Zivkovic, R., Lillquist, Y. P., Connolly, M., Hyland, K., Blau, N., Rupar, T., and Waters, P. J. Autosomal recessive GTP cyclohydrolase I deficiency without hyperphenylalaninemia: evidence of a phenotypic continuum between dominant and recessive forms. Mol.Genet.Metab 2008;94(1):127-131. View abstract.
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.

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.

This current literature is notable for its apparent irrelevancy to an AFL footballer. It begs the question; did Tβ4 make a difference to the Essendon players? The only honest answer is that we don’t know. Most of our understanding exists on a molecular and cellular level, without any significant appreciation of how Tβ4 influences applicable outcomes such as exercise performance, endurance, muscle strength, and time to recovery. Furthermore, as the majority of research has been performed on mice, rat and pig models, any results are not directly translatable to a human, let alone an elite athlete. This is a stark contrast to a supplement such as EPO, which has been investigated thoroughly.

Thymosin β4 has been tested in multicenter trials sponsored jointly by RegeneRx Biopharmaceuticals Inc (Rockville, MD, USA) and Sigma Tau (Pomezia, Italy) in the United States and Europe in patients with bed sores, ulcers caused by venostasis, and Epidermolysis bullosa simplex and was found to accelerate bed sore and stasis ulcer repair by one month. It has also been tested in patients with chronic neurotrophic corneal epithelial defects and found to promote repair.
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
Young says that the oxytocin field would benefit from closer collaboration between basic and clinical researchers. If basic scientists can work out how oxytocin helps the brain to process social stimuli, then that might help in the design of stimuli — in the form of behavioural therapies — that could be given alongside the hormone to change behaviour, just as oxytocin and pup calls together affect virgin mice. “I think in the future these two branches need to have more communication,” Young says.
Mouse BMMs were cultured with M-CSF (30 ng/mL) and RANKL (100 ng/mL) or CM collected from PDLCs for 5 days (A) and 60 minutes (B). The mRNAs expression was determined by PCR analysis (A). The phosphorylation of MAPKs (p38, JNK, and ERK), and activation of NF-κB were determined by Western blot analysis (B). Data were representative of three independent experiments. The bar graph shows the fold increase in protein or mRNA expression compared with control cells * Statistically significant differences compared with the control, p<0.05.

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.

It has been reported that deficiencies in the amino acid tryptophan (precursor to 5-HTP) are correlated with depression, as evidence by serum tryptophan in depressed persons.[16][17] Decreased levels of tryptophan in the body can come from various means but are most likely caused by a diet lacking in the amino acid as substrate, or by upregulation of enzymes (most notably indoleamine 2,3-dioxygenase(IDO) and tryptophan 2,3-dioxygenase(TDO)) that degrade tryptophan or direct it to paths that are not serotonin synthesis causing a relative deficiency.[18][19] These enzymes can be upregulated in states of chronic inflammation[18][20] and injection of some pro-inflammatory cytokines has been implicated in depression[21] and increasing the kyurenine:tryptophan ratio, which is indicative of IDO activity being increased.[22] The activity of tryptophan hydroxylase can also be further downregulated in cases of Magnesium or vitamin B6 deficiency, stress, or excessive tryptophan levels.[7]

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.
Melanotan II first captured the public's imagination when the mainstream media briefly touted it as a Viagra-like panacea for middle-aged men. Norman Levine, a dermatologist who led the team that developed the drug, had first conducted experiments in which he darkened the pigments of frogs by injecting them with a hormone called Alpha MSH. After Melanotan II was modified for human use and put through clinical trials, Levine reported that "one very astute observer who took this drug told us that he was developing spontaneous erections."
A Risk Quiz; Let’s say you are one of the volunteers to whom researchers gave $100, and this option: you can either keep the money, or give it to an anonymous trustee who will either invest it and double it to $200 and return half of the extra hundred bucks to you–$50–or keep all the money for herself. So you can either increase your money by 50%, or lose it all. What would you do? Would you trust that anonymous trustee? (Remember Loss Aversion from Chapter Two, where in a similar experiment most people decided to avoid the gamble and take the sure cash.)
Jump up ^ Grottesi A, Sette M, Palamara T, Rotilio G, Garaci E, Paci M (1998). "The conformation of peptide thymosin alpha 1 in solution and in a membrane-like environment by circular dichroism and NMR spectroscopy. A possible model for its interaction with the lymphocyte membrane". Peptides. 19 (10): 1731–8. doi:10.1016/S0196-9781(98)00132-6. PMID 9880079.

But returning hunters also need to share meat with their families and friends; this is where oxytocin comes into play. It can help overcome the potentially negative social effects of testosterone. Men who were absent for longer seem to need more oxytocin to reconnect with their families; it seems that absence does indeed make the heart grow fonder, via an oxytocin blast.
We think that the most important region is the nucleus accumbens, which is kind of up here. The nucleus accumbens is where we can measure a release of the neurotransmitter dopamine when humans or animals take drugs or are exposed to other rewarding stimuli, such as sex. Or gambling, for example, or monetary reward activates the nucleus accumbens as well.
Serotonin influences sleep and sleep-wake cycles in many ways, and scientists continue to make discoveries about how this important neurochemical affects our sleeping and waking lives. One important way serotonin affects sleep and bio time is through its relationship with the “sleep hormone” melatonin. Melatonin is made from serotonin in the presence of darkness. (Remember, melatonin production in the body is triggered by darkness and suppressed by exposure to natural and artificial light.) Healthy serotonin levels are essential for maintaining healthy melatonin levels—and both serotonin and melatonin are critical to sleep and a well-functioning bio clock. With its ability to increase serotonin, 5-HTP supports a neurochemical process that can enable high-quality sleep and keep the body’s bio clock in sync.
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.
A: While it is possible there is an interaction, it most likely is not severe or life-threatening. Keep in mind that the "T" in HTP stands for tryptophane, which is an essential amino acid that your body processes routinely. The most common interaction involved with 5-HTP is with antidepressants or other medications that are intended to affect brain chemistry, as 5-HTP is converted into serotonin, an important brain chemical that helps regulate mood.
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.
Research in the early 1960s showed that in rats, administration of α-MSH caused sexual arousal, and work on this continued in many labs up through the 1980s, when scientists at University of Arizona began attempting to develop α-MSH and analogs as potential sunless tanning agents, and synthesized and tested several analogs, including melanotan-I and melanotan II.[6][9]
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).
Much of human behavior is influenced by hormones. There’s cortisol, involved in our stress response and energy balance. Testosterone, a male sex hormone, tends to make men more competitive. Oxytocin has various social and physiological functions in the brain and the body, but is sometimes referred to as the “love hormone” due to its role in social bonding. These are all simplifications, but hormones do underlie many aspects of what we do and what we feel.
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
Work with cell cultures and experiments with animals have shown that administration of thymosin β4 can promote migration of cells, formation of blood vessels, maturation of stem cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. These multiple properties have provided the impetus for a worldwide series of on-going clinical trials of potential effectiveness of thymosin β4 in promoting repair of wounds in skin, cornea and heart.[17]
In 2015 I found my self bed ridden for 8 weeks with an issue all the doctors I had been to we’re unable to diagnose. I discovered, after much research, that what I was suffering from was damaged facia in my left and right gluteus muscles, which left me unable to do anything. I was in excruciating pain and couldn’t do anything except lay in bed on my back. Then my husband found TB 500. Initially I was against using it but after deteriorating to the point of being bed ridden I broke down and ordered some. As soon as I received it my husband injected me in the gluteus muscle. Within 30 minutes I started getting relief from the TB-500, within 8 weeks I was out of bed and the pain was gone! It healed the damaged fascia covering the gluteus. If I had not done this I don’t know where I would be today. For me, TB-500 was a life saver and if I had to I would use it again. I have suffered no side affects then or now.
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]
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.
Jump up ^ Venkatesh B, Si-Hoe SL, Murphy D, Brenner S (November 1997). "Transgenic rats reveal functional conservation of regulatory controls between the Fugu isotocin and rat oxytocin genes". Proceedings of the National Academy of Sciences of the United States of America. 94 (23): 12462–6. Bibcode:1997PNAS...9412462V. doi:10.1073/pnas.94.23.12462. PMC 25001. PMID 9356472.
Mental health is so under-funded in the UK that pills can be used as the quick-fix option. In 2014/15, 57.8million prescriptions for antidepressants or SSRIs are filled out in England alone. You can wait months on a waiting list for cognitive behavioural therapy or to see a psychiatrist, and as you wait, medication is a lifeline. In addition to this mess, pharma giants have stopped looking for the 'next Prozac', cutting funding into new treatments by 70 percent in the last decade. The bottom line is clear: SSRIs, with all their pros and cons, are here to stay.
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.

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.

Autism: Oxytocin has been implicated in the etiology of autism, with one report suggesting autism is correlated with genomic deletion of the gene containing the oxytocin receptor gene (OXTR). Studies involving Caucasian and Finnish samples and Chinese Han families provide support for the relationship of OXTR with autism.[55][56] Autism may also be associated with an aberrant methylation of OXTR.[55]
Tb4 has other effects that are needed in healing and repair of damaged tissue. It is a chemo-attractant for cells, stimulates new blood vessel growth (angiogenesis), downregulates cytokines and reduces inflammation, thus protecting newly formed tissue from damaging inflammatory events. Tb4 has been shown to reduce free radical levels (with similar efficiency as superoxide dismutase), decrease lipid peroxidation, inhibit interleukin 1 and other cytokines, and decrease inflammatory thromboxane (TxB2) and prostaglandin (PGF2 alpha).
Mental health is so under-funded in the UK that pills can be used as the quick-fix option. In 2014/15, 57.8million prescriptions for antidepressants or SSRIs are filled out in England alone. You can wait months on a waiting list for cognitive behavioural therapy or to see a psychiatrist, and as you wait, medication is a lifeline. In addition to this mess, pharma giants have stopped looking for the 'next Prozac', cutting funding into new treatments by 70 percent in the last decade. The bottom line is clear: SSRIs, with all their pros and cons, are here to stay.
It turns out oxytocin is responsible for a lot more than just love. New science has found that this amazing molecule also influences how sociable each of us is, allowing us to 'tune in' to the social information around us, perceiving it in much higher resolution. Scientists are now applying this new knowledge in the lab, and as reporter Dr Graham Phillips finds out, they're discovering oxytocin's great potential to treat social disorders, like drug addiction and alcoholism.
Synthetic oxytocin is sold as medication under the trade names Pitocin and Syntocinon and also as generic oxytocin. Oxytocin is destroyed in the gastrointestinal tract, and therefore must be administered by injection or as nasal spray. Oxytocin has a half-life of typically about three minutes in the blood. Oxytocin given intravenously does not enter the brain in significant quantities - it is excluded from the brain by the blood-brain barrier. There is no evidence for significant CNS entry of oxytocin by nasal spray. Oxytocin nasal sprays have been used to stimulate breastfeeding but the efficacy of this approach is doubtful[24].
You must be over 18 years of age to order or purchase from our website. You may not purchase this peptide for anyone who is under 18 years of age.Products are not drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. The purchaser is fully aware of the health hazards associated with these products and agrees that they are experienced in their handling.

Potential side effects of 5-HTP include heartburn, stomach pain, nausea, vomiting, diarrhea, drowsiness, sexual problems, vivid dreams or nightmares, and muscle problems.[19] Because 5-HTP has not been thoroughly studied in a clinical setting, possible side effects and interactions with other drugs are not well known. According to the US National Institute of Health TOXNET, 5-HTP has not been associated with serotonin syndrome or any serious adverse events in humans.[20] Across multiple studies, 5-HTP also been reported to not cause any noticeable hematological or cardiovascular changes.[21] 5-HTP also has not been associated with eosinophilia.[22]