In 2015 I found my self bed ridden for 8 weeks with an issue all the doctors I had been to we’re unable to diagnose. I discovered, after much research, that what I was suffering from was damaged facia in my left and right gluteus muscles, which left me unable to do anything. I was in excruciating pain and couldn’t do anything except lay in bed on my back. Then my husband found TB 500. Initially I was against using it but after deteriorating to the point of being bed ridden I broke down and ordered some. As soon as I received it my husband injected me in the gluteus muscle. Within 30 minutes I started getting relief from the TB-500, within 8 weeks I was out of bed and the pain was gone! It healed the damaged fascia covering the gluteus. If I had not done this I don’t know where I would be today. For me, TB-500 was a life saver and if I had to I would use it again. I have suffered no side affects then or now.
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.
Another interesting agent reported to significantly accelerate chronic wound repair is infrared (700–1200 nm wavelength) and near infrared (600–700 nm) light delivered through lasers or light-emitting diodes (LEDs) (Mester et al., 1968; Rochkind et al., 1989; Conlan, 1996; Schindl et al., 2000; Enwemeka, 2004). Spectroscopic measurements indicate that photons at wavelengths of 630–800 nm penetrate through the skin and muscles of the forearm and lower leg (Chance et al., 1988; Beauvoit et al., 1994, 1995). The effect of the light may be to stimulate cytochrome c oxidase in the mitochondria, resulting in increased oxygen consumption and production of ATP (Karu, 1999).
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Second, 5-HTP can cause serious drug interactions with many medications, especially those used to treat depression. Because antidepressants generally work by increasing serotonin in the brain, 5-HTP could combine with these medications to cause high concentrations of serotonin. Having too much serotonin can lead to serotonin syndrome, a serious condition characterized by dangerously high heart rate, blood pressure, and temperature. 5-HTP can interact with other classes of drugs, like migraine and pain medications, that also affect serotonin concentrations.
The activity of the PAM enzyme system is dependent upon vitamin C (ascorbate), which is a necessary vitamin cofactor. By chance, sodium ascorbate by itself was found to stimulate the production of oxytocin from ovarian tissue over a range of concentrations in a dose-dependent manner.[23] Many of the same tissues (e.g. ovaries, testes, eyes, adrenals, placenta, thymus, pancreas) where PAM (and oxytocin by default) is found are also known to store higher concentrations of vitamin C.[24]
5-HTP increases a chemical in the brain. This chemical is called serotonin. Some medications used for depression also increase serotonin. Taking 5-HTP with these medications used for depression might cause there to be too much serotonin. This could cause serious side effects including heart problems, shivering, and anxiety.

Some of these medications used for depression include phenelzine (Nardil), tranylcypromine (Parnate), and others.

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).
Oxytocin is a hormone that also acts as a neurotransmitter in the brain. Some popular media have incorrectly labeled it the “love hormone,” because it is associated with good feelings and emotions. But its role in the body is much more complex than that. It is not a bliss or hug hormone, but it does appear to be connected to human emotions and the regulation of childbirth and breast-feeding.
The relationship between oxytocin and human sexual response is unclear. At least two non-controlled studies have found increases in plasma oxytocin at orgasm in both men and women.[5][6] The authors of one of these studies speculated that oxytocin's effects on muscle contractibility may facilitate sperm and egg transport.[5] Murphy et al. (1987), studying men, found that oxytocin levels were raised throughout sexual arousal and there was no acute increase at orgasm. [7] A more recent study of men found an increase in plasma oxytocin immediantly after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted that these changes "may simply reflect contractile properties on reproductive tissue."[8]
Stimulation of uterine smooth muscle contraction at birth: At the end of gestation, the uterus must contract vigorously and for a prolonged period of time in order to deliver the fetus. During the later stages of gestation, there is an increase in abundance of oxytocin receptors on uterine smooth muscle cells, which is associated with increased "irritability" of the uterus (and sometimes the mother as well). Oxytocin is released during labor when the fetus stimulates the cervix and vagina, and it enhances contraction of uterine smooth muscle to facilitate parturition or birth. 

When combined with antidepressants of the MAOI or SSRI class, very high parenteral doses of 5-HTP can cause acute serotonin syndrome in rats.[23][24] It is unclear if such findings have clinical relevance, as most drugs will cause serious adverse events or death in rodents at very high doses. In humans 5-HTP has never been clinically associated with serotonin syndrome, although 5-HTP can precipitate mania when added to an MAOI.[25]