I was in a bad accident 5 years ago and was feeling better until my Dr. gave me levaquin which damages your mitochondria, gut, tendons And ligaments. I was going to order BPC 157 but see where you think TB500 is stronger. Do you know if it shows up on an employee drug test as i get tested occasionally? Also, your thoughts on fragment 176-191, a friend of mine uses it and suggested it for me. I understand you’re not a Dr, but just looking for your personal opinion. Thank you
Supplementation of 5-HTP has been shown to be more effective than tryptophan supplementation alone. This additional benefit of 5-HTP supplementation arises because 5-HTP bypasses the cell's L-tryptophan's own self-regulation on the IDO enzyme, in which it upregulates the activity of IDO (discussed in next section) to maintain body homeostasis of tryptophan[6] and it bypasses the tryptophan hydroxylase enzyme, which is the rate limiting step in serotonin biosynthesis.[7]
Growing up, Joe was plagued with a myriad of health issues such as gut problems, autoimmune issues, chronic fatigue, brain fog, insomnia, and general inflammation. Both conventional and alternative doctors weren’t able to help him, so he decided to fix himself. With lots of health questions and few satisfying answers, Joe decided to read every research paper he could get his hands on and conduct thousands of experiments on his own body in order to fix his health issues. Joe started SelfHacked in late 2013 when he successfully fixed all of his issues, and now it gets millions of readers a month looking to educate themselves about how they can improve their health. Joe is now a thriving author, speaker, and serial entrepreneur, founding SelfDecode & LabTestAnalyzer.
If the two things you can't live without are a dark, even tan and a fast-acting, long-lasting erection, then add Melanotan II to your holiday shopping list. This synthetic peptide hormone, which was developed by a research team at the University of Arizona during the late 1990s, darkens skin pigment and may stimulate erectile activity. And despite continued concern and controversy within the medical community regarding its use, it remains available for sale over the internet in a powdered form that can then be reconstituted for subcutaneous injections.
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.

It should be noted that supplemental 5-HTP can cause an increase in urinary 5-HIAA, which is the major metabolite of serotonin that is excreted in the urine. Increased urinary 5-HIAA is also sometimes a diagonistic marker for carcinoid tumors due to increased conversion of tryptophan to serotonin in these tumors,[62][63] and in this case serum chromogranin A should be measured (as supplemental 5-HTP does not appear to increase chromogranin A).[63]

In November 2008, the UK Medicines and Healthcare products Regulatory Agency (MHRA) warned the public against melanotan use stating it was an unlicensed medicine that may not be safe. As such, it is illegal to market or supply this product in the UK due to its unlicensed nature. Additionally the MHRA warned 18 companies about selling or advertising the product and closed down 72 websites involving melanotan. By 2013, the MHRA had received 18 reports of 74 separate reactions to the products and reactions have involved stomach and heart problems, as well as blood and eye disorders.
5-HTP, along with other L-Tryptophan supplements, have been implicated in the flu-like, potentially fatal Eosinophilic Myalgia Syndrome. This syndrome was initially tied to  impurities - Amino Acids called "Peak E" and "Peak X" - which were present in these products because of poor manufacturing processes by a single major supplier. Some people reject this idea and believe that the syndrome is caused by an excess of tryptophan itself (10, 11).

5-HTP has been linked in very rare instances to a condition known as EMS, or eosinophilia-myalgia syndrome, which combines extreme muscle tenderness with abnormalities in the blood. A contaminant that was found in some tryptophan supplements in the late 1980s, and was linked to a small number of EMS cases, was also found in some 5-HTP supplements.  It’s important to talk with your doctor before you begin taking 5-HTP or any other supplement, and to make sure you’re getting your supplements from a reliable provider.  

Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all Phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta4 (Tβ4) is the major G-actin-sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including anti-apoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.

When you get your TB-500, it will come in a powder form. Just like BPC-157, you will need to “reconstitute” it by adding bacteriostatic water. Go back and read my article on BPC-157 to get access to a peptide calculator that will help you with the mixing/dosage math. Once your TB-500 is properly mixed, you then draw the dose into an insulin syringe, and inject it intramuscularly, subcutaneously, or intravenously (according to your preference).


One way to clarify that question is to give individuals oxytocin rather than just measure naturally occurring levels. In experiments by couple therapist and researcher Beate Ditzen at the University of Zurich, couples each sprayed a liquid containing oxytocin up their noses (which ensures that the hormone reaches the brain). Ditzen then got them to talk with each other about an issue that both partners said often lead to disagreement or fighting, such as who did the housework or how they spent their free time. She observed how they communicated with each other during the discussion compared with couples who didn’t get the hormone.
A study using an oral cavity spray of 5-HTP (via the plant source of Griffonia Simplicifolia) has noted that 7.68mg of 5-HTP via 30.72mg of Griffonia Simplicifolia extract taken five times daily (total daily dose of around 40mg) has confirmed an increase in urinary 5-HIAA (from 3.71+/-1.27mg/24 hours to 8.80+/-4.02mg/24 hours; a 137% increase) relative to baseline, confirming that 5-HTP can be absorbed sublingually.[3] Similar results have been noted elsewhere with this spray, although it should be noted that it is confounded with other herbs (detailed in the appetite subsection).[2]
Neurovascular units within the central nervous system consist of endothelial cells, pericytes, neurons and glial cells, as well as growth factors and extracellular matrix proteins that are close to the endothelium.72,73 Neurovascular units provide niches for neural stem/progenitor cells in the adult brain and, within these units, newly-generated immature neurons are closely associated with the remodeling vasculature. The generation of new vasculature facilitates several coupled neurorestorative processes including neurogenesis and synaptogenesis, which improve functional recovery.74-76 The vascular production of stromal-derived factor 1 and angiopoietin 1 is involved in neurogenesis and promotes behavioral recovery after stroke.77 The disruption of this neurovascular coordination has been observed in a variety of brain conditions including infection, stroke and trauma.78 The injured brain promotes angiogenesis and neurogenesis,13,32,69,79-84 that may contribute to spontaneous functional recovery from injuries such as stroke and TBI. Neurorestorative agents that increase angiogenesis and neurogenesis have been shown to improve functional outcome following brain injury.19,33 Vascular endothelial cells within the neurovascular niche affect neurogenesis directly via contact with neural progenitor cells, while soluble factors from the vascular system that are released into the CNS enhance neurogenesis via paracrine signaling.85 Here, we demonstrate that Tβ4 treatment promotes both angiogenesis and neurogenesis in rats after TBI, suggesting that the neurovascular remodeling at least partially contributes to Tβ4-mediated improvement in functional recovery. A better understanding of molecular mechanisms in the neurovascular niches will be important for developing novel angiogenic and neurogenic therapies for brain injuries.
Affecting generosity by increasing empathy during perspective taking. In a neuroeconomics experiment, intranasal oxytocin increased generosity in the Ultimatum Game by 80% but has no effect in the Dictator Game that measures altruism. Perspective-taking is not required in the Dictator Game, but the researchers in this experimental explicitly induced perspective-taking in the Ultimatum Game by not identifying to participants which role they would be in.[20]

The CCI model we used causes cortical tissue loss. Traditionally, the target for neuroprotective treatment of TBI is to reduce the lesion volume.39,40 A major limitation of neuroprotection strategies is the short time window between injury and treatment. In the vast majority of preclinical TBI studies, the treatment compounds provide neuroprotection only when administered early (usually several hours after brain injury).11 The administration of a compound early in the clinical setting is not practical.41 The neuroprotective effects demonstrated in rodents may diminish if the treatment compounds are given in the clinical setting beyond the short neuroprotective window. We are able to stimulate recovery of neurological function without altering the lesion volume, which has also been demonstrated in our experimental studies of stroke,19,42,43 and is in essence, enhancement of neurorecovery.19 The extended 24-hour window for treatment which improves neurological recovery, without altering CCI cortical volume, is a major benefit of the neurorestorative therapy. Recently, we evaluated the efficacy of delayed Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by CCI.34 Briefly, TBI rats received Tβ4 at a dose of 6 mg/kg or a vehicle (saline) administered i.p. starting at 24 hours after injury and then every third day for 2 weeks. The dose of Tβ4 was selected based on our previous studies in animal models of stroke and EAE.25,27 Tβ4 did not alter lesion volume (14.2 ± 3.9% for saline treatment vs. 15.7 ± 3.6% for Tβ4 treatment). TBI caused neuronal cell loss in the ipsilateral CA3 and DG examined 35 days after injury compared to sham controls. Tβ4 treatment initiated 24 hours post injury significantly reduced cell loss in these two regions compared to saline controls. Tβ4-treated TBI rats showed significant improvement in spatial learning (MWM test) and sensorimotor (mNSS test) functional recovery compared to the saline-treated TBI rats.34

Despite this, Tβ4’s place on the banned-substances list is warranted. It reflects the possibility that the effects of the supplement may manifest as a tangible improvement in athletes. However, any time a journalist flippantly declares it “heals damaged tissue and speeds recovery”, it should be noted that such claims are a harmful distortion of the facts.

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.

“Further analysis by gender revealed that females in the 5-HTP group had a significantly lower panic rate and intensity of cognitive symptoms whereas, in males, the effect of 5-HTP was limited to lowering the intensity of somatic panic symptoms. Thus, an increased availability of 5-HT may have a gender-dependent protective effect in CCK-4-induced panic.”

The reason for the difference is the density of oxytocin receptors in the brain. Life pair bonders, like prairie voles or, indeed, ourselves, have a high density of receptors in the reward centre of the brain. Non-pair bonders, like meadow voles, certainly enjoy sex, but their lower density of receptors means it doesn't matter so much who the partner is. So it's not the oxytocin itself making sex enjoyable. What it's doing is influencing our mating behaviour.
But like most peptides on the market, TB-500 has limited long term studies involving human use. Although I haven’t personally used TB-500 (I can’t, since I compete in WADA sanctioned sports like triathlon and obstacle course racing), from what I’ve seen and heard from bodybuilders and athletes using the peptide, the primary side effect is a temporary sense of lethargy. Also, some people report getting a head rush when injecting TB-500, but report this head rush goes away a few minutes after injecting.

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]


Members agreed that the relevant matters under Section 52E(1) of the Therapeutic Goods Act 1989 included: (a) risks and benefits of the use of a substance; (b) the purpose for which a substance is to be used and the and extent of use; (c) the toxicity of a 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.
The 2nd purpose of this system is to provide a private and reliable environment for our customers. All communication and information here is encrypted. When orders are finalized, all data is deleted and no history is kept. The system never sends any emails. To communicate with us you will need to log in, send us a message and later check back for a reply. We usually reply within a few hours.
Since Wnt5a expression is associated with rheumatoid arthritis and periodontitis [25, 26], expression of Wnt5a and its cell surface receptors, Frizzled and receptor tyrosine kinase-like orphan receptor 2 (Ror2), were examined. As shown in Fig 9A–9D, mRNA and protein expressions of Wnt5a and its receptors were increased by H2O2 in a time- and dose-dependent manner.
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all Phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta4 (Tβ4) is the major G-actin-sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including anti-apoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.
Angiogenesis is an essential step in the repair process that occurs after injury. In this study, we investigated whether the angiogenic thymic peptide thymosin beta4 (Tbeta4) enhanced wound healing in a rat full thickness wound model. Addition of Tbeta4 topically or intraperitoneally increased reepithelialization by 42% over saline controls at 4 d and by as much as 61% at 7 d post-wounding. Treated wounds also contracted at least 11% more than controls by day 7. Increased collagen deposition and angiogenesis were observed in the treated wounds. We also found that Tbeta4 stimulated keratinocyte migration in the Boyden chamber assay. After 4-5 h, migration was stimulated 2-3-fold over migration with medium alone when as little as 10 pg of Tbeta4 was added to the assay. These results suggest that Tbeta4 is a potent wound healing factor with multiple activities that may be useful in the clinic.
In this study, Tβ4 mRNA down-regulation was detected in in vitro in PDLCs stimulated with the ROS. This down-regulation of Tβ4 was also observed in GCF of periodontitis patient [19] and endotoxin-induced septic shock of rats [39]. ROS were generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and involved in tissue destruction associated with periodontal diseases [40]. Thus, we chose to use ROS-stimulated PDLCs in this study since ROS, such as superoxide and H2O2, have been proposed as key players in bone resorption [41] and implicated in the pathogenesis of rheumatoid arthritis and periodontitis [29].
"There was no substance labelled unfit for human use so anyone that tries to bandy that comment around apart from the fact the comment is totally false, we are now starting to accrue our legal case against people that have suggested as such. Under no circumstances was anything ever injected or given to a player which was unfit for human consumption," Dank told ABC News Radio on Sunday.
Ok Ben. Thanks. Started the TB 500 for my elbows. Got the 5mg of TB 500 and reconstituted it with 3 cc/ml. of water (3 syringes full) Just about filled the file. Now based on injecting just under .1 cc/ml or just under 10 (8) units for a dose of around 250. How long did that vial last you? Seems like there is a lot left and the amount injected is small. Is my dose and math right?
Although maternal bonding may not always be hardwired — after all, human females can adopt babies and take care of them — oxytocin released during pregnancy "does seem to have a role in motivation and feelings of connectedness to a baby," Young said. Studies also show that interacting with a baby causes the infant's own oxytocin levels to increase, he added. 
^ Jump up to: a b Marazziti D, Dell'Osso B, Baroni S, Mungai F, Catena M, Rucci P, Albanese F, Giannaccini G, Betti L, Fabbrini L, Italiani P, Del Debbio A, Lucacchini A, Dell'Osso L (October 2006). "A relationship between oxytocin and anxiety of romantic attachment". Clinical Practice and Epidemiology in Mental Health. 2 (1): 28. doi:10.1186/1745-0179-2-28. PMC 1621060. PMID 17034623.
“The study is kind of a high-water mark for the field, putting different levels all together: a robust behaviour, a brain region, and a cellular basis for it,” says Richard Tsien, a neuroscientist also at Langone. Tsien has been studying the action of oxytocin on neuronal circuits in detail, by examining slices of the hippocampus, a region involved in learning and memory. In a 2013 study6 of rats, Tsien's team found that oxytocin selectively acts on a type of cell called an inhibitory interneuron in a way that quiets background chatter within the neuronal circuit. “Oxytocin improved signal transmission, almost doubling the ability of information to flow through the system,” Tsien says. In effect, it is producing more signal and less noise.
Research shows that co-administration with carbidopa greatly increases plasma 5-HTP levels.[46] However, several studies have reported that 5-HTP is effective even without a peripheral decarboxylase inhibitor (e.g. carbidopa).[47][unreliable medical source?] Other studies have indicated the risk of a scleroderma-like condition resulting from the combination of 5-HTP and carbidopa.[48]
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