^ Jump up to: a b Low TL, Hu SK, Goldstein AL (February 1981). "Complete amino acid sequence of bovine thymosin beta 4: a thymic hormone that induces terminal deoxynucleotidyl transferase activity in thymocyte populations". Proceedings of the National Academy of Sciences of the United States of America. 78 (2): 1162–6. Bibcode:1981PNAS...78.1162L. doi:10.1073/pnas.78.2.1162. PMC 319967. PMID 6940133.
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.
Sexual activity: The relationship between oxytocin and human sexual response is unclear. At least two uncontrolled studies have found increases in plasma oxytocin at orgasm – in both men and women.[103][104] Plasma oxytocin levels are notably increased around the time of self-stimulated orgasm and are still higher than baseline when measured five minutes after self arousal.[103] The authors of one of these studies speculated that oxytocin's effects on muscle contractibility may facilitate sperm and egg transport.[103]
At first, the mice showed an irregular smattering of neural impulses when they heard the baby's cries. Then, as the oxytocin kicked in, the signal evolved into a more orderly pattern typical of a maternal brain. The study showed in unusual detail how the hormone changed the behaviour of neurons1. “Oxytocin is helping to transform the brain, to make it respond to those pup calls,” Froemke says.
In 1999 researchers in Glasgow University found that an oxidised derivative of thymosin β4 (the sulfoxide, in which an oxygen atom is added to the methionine near the N-terminus) exerted several potentially anti-inflammatory effects on neutrophil leucocytes. It promoted their dispersion from a focus, inhibited their response to a small peptide (F-Met-Leu-Phe) which attracts them to sites of bacterial infection and lowered their adhesion to endothelial cells. (Adhesion to endothelial cells of blood vessel walls is pre-requisite for these cells to leave the bloodstream and invade infected tissue). A possible anti-inflammatory role for the β4 sulfoxide was supported by the group's finding that it counteracted artificially-induced inflammation in mice.
The oxytocin peptide is synthesized as an inactive precursor protein from the OXT gene.[18][19][20] This precursor protein also includes the oxytocin carrier protein neurophysin I.[21] The inactive precursor protein is progressively hydrolyzed into smaller fragments (one of which is neurophysin I) via a series of enzymes. The last hydrolysis that releases the active oxytocin nonapeptide is catalyzed by peptidylglycine alpha-amidating monooxygenase (PAM).[22]

Outside the brain, oxytocin-containing cells have been identified in several diverse tissues, including in females in the corpus luteum[34][35] and the placenta;[36] in males in the testicles' interstitial cells of Leydig;[37] and in both sexes in the retina,[38] the adrenal medulla,[39] the thymus[40] and the pancreas.[41] The finding of significant amounts of this classically "neurohypophysial" hormone outside the central nervous system raises many questions regarding its possible importance in these different tissues.
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.

Ultimately, this lack of literature on the drug best serves to illustrate the recklessness of Stephen Dank in committing to something so experimental in nature. Perhaps he was privy to anecdotal evidence the rest of us weren’t. The drug has been used by amateur athletes and bodybuilders, and reportedly in the equine industry. Nevertheless, any benefits are unsubstantiated, which lends to an exasperation shared by supporters as to why Dank would risk so much for a substance that potentially offers no advantage at all. As a supporter, I would have much preferred a drug that allowed us to hit a target inside 50.
Friedman, J., Roze, E., Abdenur, J. E., Chang, R., Gasperini, S., Saletti, V., Wali, G. M., Eiroa, H., Neville, B., Felice, A., Parascandalo, R., Zafeiriou, D. I., Arrabal-Fernandez, L., Dill, P., Eichler, F. S., Echenne, B., Gutierrez-Solana, L. G., Hoffmann, G. F., Hyland, K., Kusmierska, K., Tijssen, M. A., Lutz, T., Mazzuca, M., Penzien, J., Poll-The BT, Sykut-Cegielska, J., Szymanska, K., Thony, B., and Blau, N. Sepiapterin reductase deficiency: a treatable mimic of cerebral palsy. Ann Neurol. 2012;71:520-530. View abstract.
Oxytocin (Oxt; /ˌɒksɪˈtoʊsɪn/) is a peptide hormone and neuropeptide. Oxytocin is normally produced by the paraventricular nucleus of the hypothalamus and released by the posterior pituitary.[3] It plays a role in social bonding, sexual reproduction, and during and after childbirth.[4] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding.[5] This helps with birth, bonding with the baby, and milk production.[5][6] Oxytocin was discovered by Henry Dale in 1906.[7] Its molecular structure was determined in 1952.[8] Oxytocin is also used as a medication to facilitate childbirth.[9][10][11]

Our research mainly focusses on this early social experiences that people have that can be positive or negative, and that can really shape our developing brain. There have been some very interesting studies, for example, with children that grew up in Romanian orphanages. And we know that that early start, where it's really deprived from social contact and physical contact, had a massive impact. So we see that oxytocin levels, for example, are much lower than we would expect in other kids.

Though it may be unlikely to form part of any official psychiatric programme in the UK, Phil Cowen, Professor of Psychopharmacology at Oxford University, admitted that there are various groups for whom it could be helpful. "About half of people with severe depression never see a doctor anyway, so it's reasonable to think it's fine for them to treat themselves with something like a supplement. Perhaps if you had mild symptoms, a smaller dose would be helpful. I'd also prefer to prescribe things like exercise or computer-based CBT if it's that stage, though. But depression and anxiety is very different between people, that's important to keep in mind. No treatment is the same for anyone."


Virtually all vertebrates have an oxytocin-like nonapeptide hormone that supports reproductive functions and a vasopressin-like nonapeptide hormone involved in water regulation. The two genes are always located close to each other (less than 15,000 bases apart) on the same chromosome and are transcribed in opposite directions. It is thought that the two genes resulted from a gene duplication event; the ancestral gene is estimated to be about 500 million years old and is found in cyclostomes (modern members of the Agnatha).[12]


That view has led some clinicians to try oxytocin as a treatment for psychiatric conditions such as autism spectrum disorder. But the early trials have had mixed results, and scientists are now seeking a deeper understanding of oxytocin and how it works in the brain. Researchers such as Froemke are showing that the hormone boosts neuronal signals in a way that could accentuate socially relevant input such as distress calls or possibly facial expressions. And clinical researchers are starting a wave of more ambitious trials to test whether oxytocin can help some types of autism.

Thymosin beta-4 (Tβ4) is a water-soluble, 43-amino acid, and 4.9 kDa protein that was originally isolated from bovine thymus [6]. Since Tβ4 is the major actin-sequestering molecule in eukaryotic cells and is found in all cells [7], Tβ4 has multiple diverse cellular functions, including tissue development, migration, angiogenesis, and wound healing [7]. We previously reported that Tβ4-overexpressing transgenic mice, using a construct on the skin-specific keratin-5 promoter, have abnormal tooth development and enhanced stimulation of hair growth [8]. Moreover, exogenous Tβ4 has anti-inflammatory effects in the bleomycin-induced mouse model of lung fibrosis [9], tooth extraction sockets in rats [10], rat model of myocardial ischemia [11], corneal wound healing [12], wound healing of rat palatal mucosa [13], in vitro model of cultured human gingival fibroblasts [14], and cardiac fibroblasts [15]. However, the effects of Tβ4 over expression or inhibition on differentiation are controversial. Exogenous β4 peptide inhibited osteogenic differentiation but facilitated adipogenic differentiation in human bone marrow-derived-mesenchymal stem cells (MSCs) [16]. In contrast, Tβ4 inhibition by Tβ4 siRNA attenuated odontoblastic differentiation in the odontoblast-like cells, MDPC-23 [17]. Moreover, we recently demonstrated that odontoblastic differentiation was enhanced by activation of Tβ4 by Tβ4 peptide but was decreased by Tβ4 siRNA in human dental pulp cells (HDPCs) [18]. However, the effects of Tβ4 on osteoclastic differentiation have not been reported.
In 19 obese females given either placebo or 8mg/kg (weight not actually given, only BMI between 30-40 for women) daily for 5 weeks without any concurrent dietary recommendations, 5-HTP treatment was associated with a decrease in appetite and food intake (resulting in weight loss) without significantly affecting mood state.[9] This study noted that food intake was reduced from an average of 2,903kcal to 1,819kcal (62% of baseline) while placebo only reduced calories to 80%, and the 0.5kg weight loss in placebo was outperformed by a near 1.5kg loss in 5-HTP. These weight loss effects have been noted with 750mg 5-HTP over 2 weeks in overweight diabetics[10] and over 12 weeks in obese persons given 900mg 5-HTP daily (58% of baseline intake); this latter study had a 6 week trial without a diet (in which significant weight loss was only noted at week 6) followed up by coadministration with a diet where weight loss proceeded to reach an additional 3.3kg over the subsequent 6 weeks;[11] this latter study is duplicated in Medline.[12]
Jump up ^ Wermter AK, Kamp-Becker I, Hesse P, Schulte-Körne G, Strauch K, Remschmidt H (March 2010). "Evidence for the involvement of genetic variation in the oxytocin receptor gene (OXTR) in the etiology of autistic disorders on high-functioning level". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 153B (2): 629–39. doi:10.1002/ajmg.b.31032. PMID 19777562.

The short half-life (<2h)[16] of 5-HTP may inherently limit the therapeutic potential of 5-HTP,[17] as the systemic 5-HTP exposure levels will fluctuate substantially, even with relatively frequent dosing. Such exposure fluctuations are usually associated with increased adverse event burden, resulting from Cmax drug spikes, and decreased clinical efficacy resulting from sub-therapeutic exposure for large parts of the day. It has been proposed that 5-HTP dosage forms achieving prolonged delivery would be more effective,[17] as is generally the situation with short-acting active pharmaceutical ingredients.[18]

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