It’s a compound that the body needs in order to make serotonin, which is our main “happiness hormone.” Per Dr. Oz, 5-HTP floods the brain with serotonin and helps minimize stress, sadness, anger, and anxiety. “5-HTP targets specific emotions that drive us to overeat,” Dr. Bhatia explains. And as she already mentioned, 5-HTP also reduces physical hunger pangs and emotional cravings. Ideally, the body makes its own 5-HTP from the amino acid tryptophan, found in foods like turkey and bananas. (Why not just eat more turkey or take a tryptophan supplement? If you struggle with mood or weight, it can be a sign that your body has trouble converting tryptophan to 5-HTP.) Besides making it yourself, the only other way to get 5-HTP is from a supplement. One we like is the BRI 5-HTP Supplement ($16 for 120 capules, Amazon).
5-HTP works in the brain and central nervous system by increasing the production of the chemical serotonin. Serotonin can affect sleep, appetite, temperature, sexual behavior, and pain sensation. Since 5-HTP increases the synthesis of serotonin, it is used for several diseases where serotonin is believed to play an important role including depression, insomnia, obesity, and many other conditions.
Treatment of patients with hyperbaric oxygen has been shown to improve the healing of chronic lower extremity wounds of diabetic patients (Londahl et al., 2010). In a pilot study, this treatment has been shown to more than double the number of circulating vascular stem/progenitor cells in these patients by a mechanism that elevates platelet NOS activity and to stimulate recruitment of vascular progenitor cells to wounds made in their abdominal skin (Thom et al., 2011). This treatment might be combined with topical agents for even greater efficacy in healing chronic wounds.
On a personal note, 5-HTP is actually one of the 1st nootropics I ever used. When I was a teenager and would go to raves me and my friends would use 5-HTP the next day because ecstasy (MDMA) diminishes the serotonin levels. Anyone with much experience with ecstasy knows that the day(s) after can be pretty hellish because the drug so depletes your feel good neurotransmitters, 5-HTP is sort of a Biohack for this.
^ 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.

Thymosin beta 4, developed by RegeneRx Biopharmaceuticals as a pharmaceutical for the healing of wounds, is a synthetic version of the natural peptide. As Dr. Allan Goldstein emphasizes, “Tb4 represents a new class of wound healing compounds. It is not a growth factor or cytokine, but rather exhibits a number of physiological properties which include the ability to sequester and regulate actin, its potent chemotactic properties. . . and its capability to downregulate a number of inflammatory cytokines that are present in chronic wounds.” When a wound heals there are many growth factors produced in the area so that additional factors, such as those currently on the market for wound healing, may help but are not necessarily lacking. Tb4 treatment, however, adds a new dimension to wound repair by providing cells with actin as needed, for cell migration, replication and differentiation.


RegeneRX Biopharmaceuticals is focusing on the commercialization of Tb4 “For the treatment of injured tissue and non-healing wounds, to enable more rapid repair and/or tissue regeneration.” Especially needy are diabetics who suffer from poor blood circulation and loss of sensation of pain that keeps their wounds unnoticed and unattended for days, leading to ulcers that may not heal. Other hard healing wounds are pressure ulcers in patients who are bed ridden and often receive skin grafts as treatment, or reconstructive surgery.

When we asked a group of readers to test out 5-HTP to lose weight, they ate unlimited portions of healthy food and still shed up to five pounds in a week. We also talked to women who’d been using 5-HTP long term. Heather Miars started taking 5-HTP for her mood at Dr. Bhatia’s urging. “I was finally able to go off prescription antidepressants and lose 15 pounds!” recalls the 45-year-old mom. Meanwhile, Audra Holmes tried 5-HTP after developing “mood swings so wild, I was giving people whiplash,” she jokes. On 5-HTP, she says: “I didn’t have the highs and lows. I could suddenly get through the day without naps or comfort food!” She shed 50 pounds in 16 weeks. Wish you could have the same kind of success with an easy way to lose weight? As Dr. Oz put it: “5-HTP may be your pre-meal must-have!”

As reactive oxygen species (ROS) have been implicated in the pathogenesis of periodontitis [24], we examined whether H2O2 could down-regulate or up-regulate Tβ4 expression in PDLCs. As shown in Fig 1A and 1B, Tβ4 mRNA and protein expressions were down-regulated by H2O2 in a time- and concentration-dependent manner. Because maximal Tβ4 mRNA and protein expressions were achieved with 200 μM H2O2 within 48 hours in PDLCs, this concentration was used in subsequent experiments.


Double immunofluorescent staining for BrdU (red, A) and NeuN (green, B) to identify newborn neurons (yellow after merge, C) in the dentate gyrus of hippocampus from rats examined 35 days after TBI. Micrographs (D) show location of DiI injection in the CA3 region (indicated by white asterisk). In the CA3 region, axons projected from granule neurons in the dentate gyrus will take up injected DiI to their cell bodies. Co-localization (merge, H) of BrdU-positive nuclei (green, F) within retrogradely DiI labeled (red, E) granule cells were examined at 35 days after TBI. Scale bar = 25 μm (C, H). Scale bar = 50 μm (D).
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.
A and B; Mouse BMMs were cultured with 200 μM H2O2 and indicated concentrations of Tβ4 peptide in the presence of M-CSF (30 ng/mL) and RANKL (100 ng/mL). C and D; PDLCs were co-cultured with mouse BMMs in the presence of M-CSF, RANKL, 200 μM H2O2, and indicated concentrations of Tβ4 peptide. To monitor osteoclast differentiation, both TRAP activity and the number of TRAP multinucleated cells were examined. * Statistically significant difference compared with control, p<0.05. The data presented were representative of three independent experiments.
Both the production of oxytocin and response to oxytocin are modulated by circulating levels of sex steroids. The burst of oxytocin released at birth seems to be triggered in part by cervical and vaginal stimulation by the fetus, but also because of abruptly declining concentrations of progesterone. Another well-studied effect of steroid hormones is the marked increase in synthesis of uterine (myometrial) oxytocin receptors late in gestation, resulting from increasing concentrations of circulating estrogen.
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.
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(4):520-530. View abstract.
The pore-forming subunit of the cardiac sodium channel Nav1.5 encoded by SCN5A is a critical determinant of myocardial excitability and conduction. Loss-of-function mutations in SCN5A can clinically manifest as progressive cardiac conduction disorders or as arrhythmic syndromes, such as Brugada syndrome. In addition to electrophysiological dysfunction, SCN5A mutations are also associated with myocardial fibrosis manifesting as global cardiomyopathy. In a 10-year old child exhibiting Brugada syndrome, the mutation SCN5AE555X was discovered. Therefore, cardiac sodium channelopathy pig models were generated by homologous recombination in the genetic background of outbred Yucatan minipigs via SCNT exhibiting the orthologous porcine heterozygous mutation SCN5AE558X. The heterozygous mutant animals were viable and fertile, and showed no sudden death over a 2-year monitoring period. They showed reduced SCN5A protein expression, which resulted in diminished total sodium conductance. The heterozygous mutant hearts showed slowed conduction and increased susceptibility for ventricular arrhythmias in the absence of structural defects of the myocardium or specialized conduction system. In total, a novel animal model was established for understanding the mechanisms linking sodium channel dysfunction to cardiac pathophysiology (Park et al., 2015b).
These results were in agreement with previous studies that showed Wnt5a expression can be induced in activated macrophages, endothelial cells, and bone marrow mesenchymal stem cells (BMSCs) after inflammatory stimulation [58, 59]. In addition, we found that the effects of Tβ4 peptide on H2O2-mediated induction of pro-inflammatory cytokines (NO, PGE2, TNF-α, IL-1β, IL-6, IL-8, and IL-17), the expression of inflammatory mediators (iNOS and COX-2), osteoclastogenic cytokines (cathepsin-K, calcitonin receptor or Calcr, NFATc1, and RANK), and osteoclastic differentiation, were reversed by exogenous treatment with Wnt5a siRNA but enhanced by rh-Wnt5a, suggesting that the anti-inflammatory and anti-osteoclastogenetic effects of Tβ4 activation were involved the Wnt5a-dependent signaling pathway. Similar to our results, Wnt5a knock-down markedly reduced cytokine/chemokine production induced by TNF in HDPCs [60].
The soluble form of Ac-SDKP peptide, derived from thymosin beta-4, has been described as a natural inhibitor of pluripotent hematopoietic stem cell proliferation and as a stimulator of angiogenesis, both in vitro and in vivo (Koutrafouri et al., 2001; Wang et al., 2004). This peptide has been selectively bound to acrylated hyaluronic acid hydrogels via thiol groups from cysteine residues (Song et al., 2014). Unfortunately, the immobilization process was poorly characterized and the effect of hydrogels on EC function was not tested in vitro. In a mouse model of chronic myocardial infarction, hydrogels with immobilized Ac-SDKP did not show improved regeneration potential. Yet, Ac-SDKP-HA hydrogels with entrapped stem cell homing factor SDF-1 showed a significant increase of myocardial regeneration and recovery of heart function, as compared to groups with only one or none of these factors, suggesting a potentially interesting synergistic effect.
But we have to be just as good at recognizing who we can trust, so the system needs fine-tuned control. That’s apparently where oxytocin comes in. The amygdala, that critical organ for our biological risk response, has a high concentration of receptors for oxytocin. In the second set of those gambling experiments with the volunteers and the trustees, researchers used fMRI to watch the brains of the volunteers as they made their choices. As the levels of oxytocin in the brain went up compared with the placebo group, activity in the amygdala went down! Oxytocin diminishes the amygdala’s ability to send out the message “Warning! Warning! I don’t trust this guy.”
During clinic trials for its use as a tanning agent, melanotan II was found to be a potent stimulator of male erections. A new drug based on melanotan II, bremelanotide, was developed to take advantage of this property. It has been noted across several studies to increase rigidity and duration of male erection, as well as male sexual desire. It has also been shown to increase female sexual desire in patients with sexual arousal disorder.
There is also a positive feedback involved in the milk-ejection reflex. When a baby sucks at the breast of its mother, the stimulation leads to oxytocin secretion into the blood, which then causes milk to be let down into the breast. Oxytocin is also released into the brain to help stimulate further oxytocin secretion. These processes are self-limiting; production of the hormone is stopped after the baby is delivered or when the baby stops feeding.
Jump up ^ Xu J, Jian B, Chu R, Lu Z, Li Q, Dunlop J, Rosenzweig-Lipson S, McGonigle P, Levy RJ, Liang B (December 2002). "Serotonin mechanisms in heart valve disease II: the 5-HT2 receptor and its signaling pathway in aortic valve interstitial cells". The American Journal of Pathology. 161 (6): 2209–18. doi:10.1016/S0002-9440(10)64497-5. PMC 1850896. PMID 12466135.
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