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.
If you were to go on the internet, read the hype, you'd probably think it'll be something like having an ecstasy tablet or having an orgasm or something like that, but the reality is you probably wouldn't be able to distinguish it from placebo. So the effects are extremely subtle. Now, that subtlety isn't necessarily because of oxytocin itself being a subtle hormone, it's just this issue of it penetrating the brain. So when you take it intranasally, we're still trying to work out how much gets into the brain, but probably only a vanishingly small amount.
Jump up ^ Carlier MF, Hertzog M, Didry D, Renault L, Cantrelle FX, van Heijenoort C, Knossow M, Guittet E (September 2007). "Structure, function, and evolution of the beta-thymosin/WH2 (WASP-Homology2) actin-binding module". Annals of the New York Academy of Sciences. 1112: 67–75. Bibcode:2007NYASA1112...67C. doi:10.1196/annals.1415.037. PMID 17947587.
^ Jump up to: a b Hurlemann R, Patin A, Onur OA, Cohen MX, Baumgartner T, Metzler S, Dziobek I, Gallinat J, Wagner M, Maier W, Kendrick KM (April 2010). "Oxytocin enhances amygdala-dependent, socially reinforced learning and emotional empathy in humans". The Journal of Neuroscience. 30 (14): 4999–5007. doi:10.1523/JNEUROSCI.5538-09.2010. PMID 20371820.
Although Tβ4 contains only 43 amino acids, it appears to have a wide range of regenerative activities and specific sites on the molecule have been shown to mediate these effects (Goldstein & Kleinman, 2015; Sosne, Qiu, Goldstein, & Wheater, 2010). Both chemically synthesized and recombinant forms have shown efficacy for dermal healing in preclinical models and in human patients (Ehrlich & Hazard, 2012; Kim & Kwon, 2014, 2015; Malinda et al., 1999; Philp, Badamchian, et al., 2003; Philp & Kleinman, 2010; Philp et al., 2006; Ti et al., 2015; Treadwell et al., 2012). A dimeric form has been found to accelerate the rate of dermal healing in an animal model more rapidly than that of the parent molecule (Xu et al., 2013). Tβ4 has also shown repair and regenerative activity in a number of other injury models, such as traumatic brain injury, spinal cord injury, stroke, a model of multiple sclerosis, ischemic limbs, and cardiac damage due to ischemia (Bock-Marquette, Saxena, White, Dimaio, & Srivastava, 2004; Cheng, Kuang, Zhang, Ju, & Wang, 2014; Dube, Bollini, Smart, & Riley, 2012; Morris, Chopp, Zhang, Lu, & Zhang, 2010; Morris et al., 2014; Philp & Kleinman, 2010; Postrach et al., 2014; Smart et al., 2007; Sopko et al., 2011; Ti et al., 2015, Wang et al., 2012; Wei, Kim, Li, Wu, & Gupta, 2014; Xiong, Mahmood, Meng, et al., 2011; Zhang, Zhang, Morris, et al., 2009; Zuo et al., 2013). The processes and pathways for Tβ4-mediated repair are similar in these various tissues and support the observed promotion of dermal healing.
The uterine-contracting properties of the principle that would later be named oxytocin were discovered by British pharmacologist Sir Henry Hallett Dale in 1906, and its milk ejection property was described by Ott and Scott in 1910 and by Schafer and Mackenzie in 1911. In the 1920s, oxytocin and vasopressin were isolated from pituitary tissue and given their current names. The word oxytocin was coined from the term oxytocic, Greek ὀξύς, oxys, and τοκετός , toketos, meaning "quick birth".
Thank you for this important segment. i have read books that mention oxytocin along with other brain chemicals, if levels are low in the brain it will cause problems, of course, makes sense. low brain neurotransmitters can be restored by using amino acids (supplements) eg: tryptophan will increase serotonin and cure depression without the use toxic pharmaceutical drugs that don.t work.
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. However, the absence of either oxytocin or its receptor in knockout mice has not been reported to produce cardiac insufficiencies.
There are several layers in the skin; the outer epidermis and beneath it the dermis and the subcutaneous layer. Cells in the epidermis include keratinocytes, its major cell type, that move continuously from the lower basal layer where they are formed by cell division. Other cells in the epidermis are the melanocytes that synthesize pigment and transfer it to the keratinocytes, giving our skin its color, and a wide variety of immune cells that maintain immune surveillance and secrete substances called cytokines, like interleukin 1 and 2, which are active in inflammation. The dermis contains connective tissue, mainly collagen, blood vessels, various types of immune white cells and fibroblasts.
For depression: Most commonly, 150-800 mg daily is taken for 2-6 weeks. These doses are sometimes divided up and administered as 50 mg to 100 mg three times a day. Sometimes the dose starts out low and steadily increases every 1-2 weeks until a target dose is reached. Less commonly, higher doses are used. In one study, the dose is steadily increased up to 3 grams per day.
In mammals, many mysteries remain. Oxytocin is difficult to measure reliably in the brain, making it hard to know exactly where, when and how much is normally released; nor do scientists understand precisely how it works to alter behaviour. “What we need to start thinking about is the more fundamental role that oxytocin plays in the brain,” Young says. The determination to find out has been strengthened by a growing move in neuroscience to characterize circuits that are important in brain operations. “That's the level that's critical for understanding how the brain is regulating behaviour,” says Thomas Insel, director of the US National Institute of Mental Health in Bethesda, Maryland, who has studied oxytocin in voles.
Thymosin beta 4 accelerated skin wound healing in a rat model of a full thickness wound where the epithelial layer was destroyed. When Tb4 was applied topically to the wound or injected into the animal, epithelial layer restoration in the wound was increased 42% by day four and 61% by day seven, after treatment, compared to untreated. Furthermore, Tb4 stimulated collagen deposition in the wound and angiogenesis. Tb4 accelerated keratinocyte migration, resulting in the wound contracting by more than 11%, compared to untreated wounds, to close the skin gap in the wound. An analysis of skin sections (histological observations) showed that the Tb4 treated wounds healed faster than the untreated. Proof of accelerated cell migration was also seen in vitro, where Tb4 increased keratinocyte migration two to three fold, within four to five hours after treatment, compared to untreated keratinocytes.
Bone loss associated with inflammatory diseases, such as rheumatoid arthritis, periodontal disease, and osteoporosis, and elevated osteoclast activity leads to bone destruction . The most common osteolytic disease, periodontitis, is a multi-factorial irreversible and cumulative condition, initiated and propagated by bacteria and host factors . Destruction of peridontal tissue is mediated via the expression of various tissue-destructive enzymes or inflammatory mediators such as interleukins-1 (IL-1), IL-6 and IL-8, tumor necrosis factor- α (TNF- α), nitric oxide (NO), and prostaglandin E2 (PGE2) . Receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) and osteoprotegerin (OPG) are critical for homeostatic control of osteoclast activity, suggesting that they have vital roles in the progression of bone loss in periodontitis [3, 4]. Therefore, resolution of inflammation and blocking osteoclast differentiation might be a potential therapeutic approach for the prevention and treatment of osteolytic inflammatory disease, such as periodontitis .
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.
Suggested doses vary depending on the source – some sellers will encourage higher use! One site suggests starting with a dose of 0.25mg. If side-effects (see above) are not proving troublesome, the site advises users to attempt to increase daily dosage. After 2-3 weeks of daily use, or when the desired level of pigmentation has been achieved, people who use Melanotan II should start a maintenance phase of two injections per week.
Jump up ^ Vargas-Pinilla P, Paixão-Côrtes VR, Paré P, Tovo-Rodrigues L, Vieira CM, Xavier A, Comas D, Pissinatti A, Sinigaglia M, Rigo MM, Vieira GF, Lucion AB, Salzano FM, Bortolini MC (January 2015). "Evolutionary pattern in the OXT-OXTR system in primates: coevolution and positive selection footprints". Proceedings of the National Academy of Sciences of the United States of America. 112 (1): 88–93. Bibcode:2015PNAS..112...88V. doi:10.1073/pnas.1419399112. PMC 4291646. PMID 25535371.
Oxytocin is known as the hormone that promotes feelings of love, bonding and well-being. It's even being tested as an anti-anxiety drug. But new research shows oxytocin also can cause emotional pain. Oxytocin appears to be the reason stressful social situations, perhaps being bullied at school or tormented by a boss, reverberate long past the event and can trigger fear and anxiety in the future. That's because the hormone actually strengthens social memory in the brain.
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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.
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).
The idea that oxytocin is central to social cognition made it an attractive candidate for treating psychiatric disorders, especially autism spectrum disorder. People with this condition, who often have problems with social interaction and communication, may not process social stimuli appropriately — and scientists theorized that oxytocin might reverse some of the symptoms. Beginning in 2010, results emerged that seemed to support this theory: researchers found that single puffs of oxytocin could temporarily improve measures of empathy and social cooperation in people with autism spectrum disorder.
Chae, H. S., Kang, O. H., Choi, J. G., Oh, Y. C., Lee, Y. S., Jang, H. J., Kim, J. H., Park, H., Jung, K. Y., Sohn, D. H., and Kwon, D. Y. 5-hydroxytryptophan acts on the mitogen-activated protein kinase extracellular-signal regulated protein kinase pathway to modulate cyclooxygenase-2 and inducible nitric oxide synthase expression in RAW 264.7 cells. Biol Pharm Bull 2009;32(4):553-557. View abstract.