Thymosins were discovered in the mid 1960’s, when Allan Goldstein from the Laboratory of Abraham White at the Albert Einstein College of Medicine in New York studied the role of the thymus in development of the vertebrate immune system. Since then, Dr. Goldstein founded a company that creates thymosin alpha 1 for the purpose of increasing immune cell activity, and thymosin beta 4 (TB-500) to promote wound repair and healing.

Naturalistic studies like ours can help unravel the evolutionary history and function of these hormones. Basically, the fact that hormone mechanisms have been tweaked during evolution suggests that the behaviors they promote have provided fitness benefits in the past. In this case, hunting and sharing meat must have increased men’s reproductive success.
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.
Letdown reflex in lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be 'let down' into a collecting chamber, from where it can be extracted by sucking at the nipple. Sucking by the infant at the nipple is relayed by spinal nerves to the hypothalamus. The stimulation causes neurons that make oxytocin to fire action potentials in intermittent bursts; these bursts result in the secretion of pulses of oxytocin from the neurosecretory nerve terminals of the pituitary gland.
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.
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.

5-HTP is necessary for the proper functioning of your body. It is decarboxylated in the brain and liver to produce serotonin, a neurotransmitter. Serotonin is involved in the communication between nearly all of our 40 million brain cells, and is also found in large quantities in the cells of the gut, and in blood platelets. Because of its widespread distribution through the cells of the body, Serotonin is believed to have a large number of psychological and physiological effects. It has been used to treat conditions as diverse as obesity, depression, fibromyalgia, insomnia, and headaches, with varying success.


Naturalistic studies like ours can help unravel the evolutionary history and function of these hormones. Basically, the fact that hormone mechanisms have been tweaked during evolution suggests that the behaviors they promote have provided fitness benefits in the past. In this case, hunting and sharing meat must have increased men’s reproductive success.
Serotonin syndrome (Serotonin toxicity) is caused by an excess of serotonin in the brain. It is most often caused by taking more than one Serotonin-enhancing substance at the same time, such as 5-HTP and an antidepressant medication. Symptoms range in severity according to the level of intoxication and may include increased heart rate, tremor, sweating, mental agitation, seizures, shock, organ failure and death (9).
"By understanding the oxytocin system's dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions," said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.
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.
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Toxicity effects of melanotan II from therapeutic and overdose exposures include renal dysfunction, rhabdomyolysis, sympathomimetic overdrive, change in size and pigmentation of pre-existing moles, rapid increase in the number of new moles, associated with causing melanomas, posterior reversible encephalopathy syndrome, refractory priapism, stretching and yawning syndrome, shortness of breath, chest pain, abdominal cramping and pain, dizziness and lethargy.
The PDLCs were pre-treated with Wnt5a siRNA (30 nM) or Wnt5 peptide (500 ng/mL) for 2 hours, post-incubated with Tβ4 peptide (1 μg/mL) and 200 μM H2O2 for 48 hours (A-E), and then conditioned medium (CM) was collected. The bar graph shows the fold increase in protein or mRNA expression compared with control. * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2-treated group. The data presented were representative of three independent experiments.
I was just diagnosed with achilles tendonosis in both of my achilles. I am an avid lifter as well as city leagues for football and basketball, I live in Montana so I hike a lot and participate In obstacle course races. My achilles have ground me to a halt over the last 3 months months. I have been referred to a surgeon for a Tenex procedure on both achilles. I am only 32 the last thing I want is have both of my achilles cut into. I’m looking at the TB-500 and BPC-157 to hopefully avoid surgery. I have done my research but am getting conflicting numbers as far as dosing. I am roughly 240 pounds and 6’5 could u recommend a dosage and cycle? Also I was wondering where the most effective injection site would be? Do I need it directly into the achilles itself or is local good enough?
However, as I’ve said elsewhere, depression is kind of like a check engine light on car, it’s a quiet ambiguous sign that something is not working somewhere in your neurobiology. There is literally dozens (perhaps hundreds) of different ways to attempt to treat depression. Amongst the vast number of options for treating depression, there is a couple of low hanging fruits; things you would want to start with before moving onto more radical options, like…
In the experiments, an epithelial wound was made in the corneas of sedated rats. A Tb4 solution was applied at several concentrations to the injured eyes in one group of rats while another group was treated with a solution without Tb4. Following 12, 24 and 36 hours, the eyes were tested by microscopic observation for epithelial growth over the injured site. Investigators found the Tb4 accelerated corneal wound repair at doses of Tb4 similar to those found to repair skin wounds. When tested 24 hours after treatment, the rate of accelerated repair was proportional to the concentration of Tb4, with the highest dose (25 microgram) showing a threefold acceleration of epithelial cell migration, compared to untreated. Treatment with Tb4 showed anti-inflammatory effects, helping resolve the injury. An application to human cells in a model of human corneal cells in culture showed that Tb4 enhanced epithelial cell migration in vitro.
The peripheral actions of oxytocin mainly reflect secretion from the pituitary gland. The behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland, or that are collaterals from them.[31] Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala, ventromedial hypothalamus, septum, nucleus accumbens, and brainstem.[citation needed]
My physiotherapist suggested BCP-157. We injected this into the palm for a few weeks 3x week. We then worked up a 50/50 mix of BCP and TB500. I’ve upped my injections ( 5-7 injections) into the surrounding areas of the protruding nodes in my palm. The results have been significant. Into week 6 of a 3x injection program, and the chords are opening up (reacting to the ‘rematrixing’ of the cells). The TB seems to disperse the liquid throughout my palm. My ‘clutched palm’ is reduced and flexibility is restored. We’re going to stick with this for another couple of months.
Wow I wonder if it will help those of us with Ehlers Danlos Syndrome – a collagen disorder that causes ligament laxity and makes those with it prone to easy subluxations and early onset arthritis. I have so many injuries from my daily life due to this disorder. I know this won’t fix my faulty collagen since that is encoded in my genes but perhaps it would help with the symptoms – a bunch of torn ligaments and worn out joints. Thanks for sharing!
While all of the effects described above certainly occur in response to oxytocin, doubt has recently been cast on its necessity in parturition and maternal behavior. Mice that are unable to secrete oxytocin due to targeted disruptions of the oxytocin gene will mate, deliver their pups without apparent difficulty and display normal maternal behavior. However, they do show deficits in milk ejection and have subtle derangements in social behavior. It may be best to view oxytocin as a major facilitator of parturition and maternal behavior rather than a necessary component of these processes.

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.
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 usually located close to each other (less than 15,000 bases apart) on the same chromosome, and are transcribed in opposite directions (however, in fugu,[44] the homologs are further apart and transcribed in the same direction).
To determine the direct effect of Tβ4 peptide on osteoclastogenesis, mouse BMMs were directly exposed to Tβ4 peptide. Direct treatment with Tβ4 peptide also reduced the number of multinucleated TRAP-positive cells and TRAP activity in a dose-dependent manner (Fig 7A and 7B). Since Tβ4 downregulated H2O2-induced various cytokines expression, the indirect effect of Tβ4 on osteoclast formation through PDLC cells using co-culture system were investigated. After addition of Tβ4 peptide to the BMMs-PDLCs co-culture, the number of osteoclast and TRAP activity were also significantly decreased (Fig 7C and 7D).
Oral 5-HTP results in an increase in urinary 5-HIAA, a serotonin metabolite, indicating that 5-HTP is peripherally metabolized to serotonin, which is then metabolized. This might cause a false positive test in tests looking for carcinoid syndrome.[28][29] Due to the conversion of 5-HTP into serotonin by the liver, there could be a risk of heart valve disease from serotonin's effect on the heart, as based on preclinical findings.[30][31] However, 5-HTP has not been associated with cardiac toxicity in humans.[22][32][33][34]
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