Oxytocin production is controlled by a positive feedback mechanism. This mechanism allows the release of the oxytocin hormone when a trigger occurs. The hormone then causes an action in the body, such as the letdown of milk or the start of labor contractions, which signals more production of oxytocin. The feedback cycle continues until the action, such as childbirth or feeding the baby, is complete.
The molecule of this peptide is very big, so it isn’t able to completely fit within a receptor. Each area of the molecule has different functions. For instance, TB 500 is responsible for promoting majority of the useful effects, such as the healing, muscle cells, new blood and repair. In some scenarios, TB 500 could be used rather than the whole Thymosin Beta 4 protein. TB 500’s main ability is to regulate Actin, which is a cell-building protein. There are thousands of proteins found inside of cells, but actin makes up to 10 percent of the total amount of proteins, giving it a major role in the cell’s genetic makeup.
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. 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).
5-HTP is POSSIBLY SAFE when taking by mouth appropriately. 5-HTP has been used safely in doses up to 400 mg daily for up to one year. However, some people who have taken it have developed a condition called eosinophilia-myalgia syndrome (EMS), a serious condition involving extreme muscle tenderness (myalgia) and blood abnormalities (eosinophilia). Some people think EMS might be caused by an accidental ingredient or contaminant in some 5-HTP products. However, there is not enough scientific evidence to know if EMS is caused by 5-HTP, a contaminant, or some other factor. Until more is known, 5-HTP should be used cautiously.
Bartz found that when she averaged out the volunteers’ results, the sniffs of oxytocin hadn’t seemed to colour their memories of their mothers. But things changed when she looked at them individually. Those who felt more anxious about their relationships took a dimmer view of their mother’s parenting styles when they sniffed oxytocin, compared to the placebo. Those who were more secure in their relationships reacted in the opposite way – they remembered mum as being closer and more caring when they took the oxytocin.
Jump up ^ Hicks C, Ramos L, Reekie T, Misagh GH, Narlawar R, Kassiou M, McGregor IS (June 2014). "Body temperature and cardiac changes induced by peripherally administered oxytocin, vasopressin and the non-peptide oxytocin receptor agonist WAY 267,464: a biotelemetry study in rats". British Journal of Pharmacology. 171 (11): 2868–87. doi:10.1111/bph.12613. PMC 4243861. PMID 24641248.
There have been some side effects reported while using Melanotan 2, typically these effects appear during the first few days of dosing and will become increasingly less obvious as the body adjusts to the peptide. These effects include: nausea, appetite loss, drowsiness and increased sex drive. In order to combat nausea, an anti-histamine can be taken when injecting until the body gets used to it. But most common way to deal with this is to inject Melanotan before bed, this is also beneficial to combat any drowsiness.
The logic behind this trend is that creating tanned skin (by increasing melanin) with minimal to no sun exposure could protect individuals from skin damage, and even potentially lower melanoma risk. More melanin means more protection from UV radiation, and therefore a healthier (and conveniently, deeper) complexion. In this sense, there is perhaps a kernel of truth to the idea of the “healthy glow”.
Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons make other peptides, including corticotropin-releasing hormone and dynorphin, for example, that act locally. The magnocellular neurosecretory cells that make oxytocin are adjacent to magnocellular neurosecretory cells that make vasopressin. These are large neuroendocrine neurons which are excitable and can generate action potentials.
A study published last year in Biological Psychiatry was the first to assess whether people with variations in their oxytocin-receptor gene have a harder time maintaining romantic relationships than those who don’t. Hasse Walum, a graduate student at Karolinska Institute in Stockholm, and his colleagues took advantage of Swedish twin studies that included thousands of participants, their genetic information and their answers to questions about how affectionate they were with their romantic partners. They found that women with a specific variation weren’t as close to their partners as women without it: they kissed their partners less and didn’t desire physical proximity as often. These women were also more likely to report having had a marital crisis. Although researchers don’t know exactly how this variation affects the oxytocin system, it may result in a lower number of oxytocin receptors in the brain. People with fewer receptors would be less sensitive to the hormone’s effects.
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
Down syndrome. Some research shows that giving 5-HTP to infants with Down syndrome might improve muscle and activity. Other research shows that it does not improve muscle or development when taken from infancy until 3-4 years of age. Research also shows that taking 5-HTP along with conventional prescription drugs does improve development, social skills, or language skills.